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Australian Biochemist The Magazine of the Australian Society for Biochemistry and Molecular Biology Inc. December 2020, Volume 51, Number 3 ISSN 1443-0193 VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 1
Table of Contents
3 Editorial Committee
4 From the President
5 ASBMB 2020 Meeting Reports
9 Publications with Impact
Unravelling the Speciation, Trafficking, Autoinflammatory Potential of the Killer Protein, MLKL
Fluid Coupling in the Rotary Motor of Life
The Natural Function of a Multidrug Resistance Transporter
Uncovering a New Way in Which Tumours Co-opt Their Microenvironments to Promote
Disease Progression
Mutational Landscape of Gall Bladder Cancers
Structural Venomics: from Single to Double Knots and Everything in Between
19 ASBMB Education Feature
Online Lessons From Our Students – 2020 ASBMB Education Symposium
Ten Reasons to Crowdsource Exam Questions (and How to Do it Properly)
Transitioning Case-based Biochemistry Workshops to Online During COVID-19
25 SDS Page
A Beginner’s Guide to Milestone Preparation
27 Competition: Campus Visit
28 Perth Protein Group: an ASBMB Special Interest Group
29 Metabolism and Molecular Medicine: an ASBMB Special Interest Group
31 Off the Beaten Track
Follow Your Dreams, Until Something Better Comes Along
32 ASBMB Member Wins Western Australian Premier’s Science Award
34 Intellectual Property
Timing is Everything: When to Pull the Trigger on Patent Filing
37 News from the States
41 Great Expectations
It’s Not Only What You Know, It’s Who Front Cover
You Know – an Unplanned Career
ASBMB President, Joel Mackay,
45 ASBMB Member Named Melburnian delivers the opening address at the 2020
of the Year ASBMB Research Symposium held online.
45 In Memoriam
47 ASBMB Annual Reports
51 Our Sustaining Members The Australian Biochemist
Editor Tatiana Soares da Costa
56 ASBMB Council Editorial Officer Liana Friedman
57 Directory © 2020 Australian Society for Biochemistry
and Molecular Biology Inc. All rights reserved.
PAGE 2 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020
Australian Biochemist Editorial Committee
Editor Editorial Officer
Dr Tatiana Soares da Costa Liana Friedman
Department of Biochemistry and Email: liana.friedman@monash.edu
Genetics
La Trobe Institute for Molecular
Science
La Trobe University
Bundoora VIC 3086
Email: editor@asbmb.org.au
Phone: (03) 9479 2227
Dr Doug Fairlie Dr Sarah Hennebry
Olivia Newton-John Cancer FPA Patent Attorneys
Research Institute and La Trobe 101 Collins Street
University Melbourne VIC 3000
Heidelberg VIC 3084 Email: sarah.hennebry@
Email: doug.fairlie@onjcri.org.au fpapatents.com
Phone: (03) 9496 9369 Phone: (03) 9288 1213
Joe Kaczmarski Associate Professor Tracey Kuit
Research School of Chemistry School of Chemistry and Molecular
Australian National University Bioscience
Canberra ACT 0200 University of Wollongong
Email: joe.kaczmarski@ Wollongong NSW 2522
anu.edu.au Email: tracey_kuit@uow.edu.au
Phone: (02) 4221 4916
Dr Erinna Lee Dr Nirma Samarawickrema
La Trobe Institute for Molecular Department of Biochemistry and
Science and Olivia Newton-John Molecular Biology
Cancer Research Institute Monash University
Heidelberg VIC 3084 Clayton VIC 3800
Email: erinna.lee@latrobe.edu.au Email: nirma.samarawickrema@
Phone: (03) 9496 9369 monash.edu
Phone: (03) 9902 0295
Dr Gabrielle Watson
Monash Biomedicine Discovery
Institute
Monash University
Clayton VIC 3800
Email: gabrielle.watson@
monash.edu
Phone: (03) 9902 9227
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 3
From the President
This piece is my swan song as ASBMB President, as One of our aims this
I hand over the reins to Jacqui Matthews for the next year was to increase our
two years. Jacqui will be well known to many of you involvement in science
in the Australian biochemistry and molecular biology advocacy. We achieved
community, particularly those of you who attend the an important first step in
Lorne Conference on Protein Structure and Function. that direction – Tatiana
Jacqui has just finished up her term as Chair of that Soares da Costa has
meeting and was obviously looking for a new challenge! recently been elected to
The last two years have seen some change at the the board of Science and
ASBMB, particularly in our trialling of a new Society Technology Australia
conference timetable. We decided to host an ASBMB- (STA) – the advocacy
focussed meeting every two years and have ComBio group that represents
only in the alternate years. We thought this might offer over 80,000 STEM
members the opportunity to meet in a more intimate professionals, including
venue than one of the large convention centres that we ASBMB’s members, to government – as the Biological
need to use for ComBio meetings. Sciences Cluster Representative. We look forward to
Our first ASBMB-only meeting was held in Perth in hearing from her about the role and about what we
October 2019. Nic Taylor from the University of Western can do to further the cause of science on the political
Australia put a huge effort into coordinating a team to agenda in Australia.
run this meeting. The overall consensus amongst the What else have I been trying to do during my term as
attendees was that it was a very enjoyable meeting with President? We have done quite a bit of ‘internal’ work,
a good atmosphere and a great program. Attendance clarifying guidelines for State Representatives and
at the meeting was lower than we would have hoped Special Interest Groups, providing State Representatives
for, no doubt in part due to it being situated on the with a forum to connect with each other on a regular
west coast, and possibly also partly due to uncertainty basis to exchange ideas, and reinvigorating the website
on our part about the best way to focus the topics of (thanks to our webmaster Liana Friedman!). I would
the meeting. When we were planning the meeting, we still like to survey members about the Society and to
thought that highlighting a small number of topics in the consider whether we should coordinate an annual
program (while still allowing talks in any subject area) meeting of Heads of Discipline in our field, as a way to
might attract more attendees. With hindsight, we may share knowledge. I am hoping to organise these things
have been wiser to not showcase particular subject before the end of 2020.
areas, as it might have given the impression that other I’d like to finish off by giving enormous thanks to the
topics would not be covered at all during the meeting. people who have contributed to ASBMB during my time
We are still keen to see if we can get the ASBMB-only as President and who, without exception, have been
format to work – scientifically and financially – and I think inspired, efficient, thorough and good humoured. Briony
we will try to cast the net wider in future incarnations of Forbes and Dominic Ng have been stalwart Secretaries,
the meeting. We will also seek feedback from members Marc Kvansakul has been a trustworthy Treasurer,
to gauge their thoughts on meeting formats. Tatiana Soares da Costa, an energetic Editor (and
Speaking of meetings, the online ASBMB symposia savvy social media specialist – follow @ITSASBMB on
in September were a real success and it makes me Twitter), Liana Friedman, our expert Webmaster and
wonder whether we could continue the momentum Editorial Officer, and Leann Tilley as Past President.
with that format of having one or more short online And of course, Sally and Chris Jay have been the
meetings (or even mixed live plus online, once that’s consummate professionals who have continued to hold
permitted) as part of our regular offering (alongside it all together for us at the National Office – and have
face-to-face conferences). I know most of us prefer the engaged with our ever-valuable Sustaining Members.
face-to-face format, but there are some advantages in Jackie Wilce and Mark Hulett have allowed me to not
terms of ease of organisation, low cost of attendance be concerned at all about the next ComBio, by doing
and the opportunity to give more members a chance to a superb job of organising the one that will be held in
present their work (particularly ECRs). The Education- Melbourne in 2022 (and locking in the 2020 Nobel Prize
focussed meeting was particularly well attended, and in Chemistry Jennifer Doudna as a keynote speaker).
I really would like to see us take advantage of that Leann has also strengthened our conference portfolio
success to create a regular forum for presentations by leading a team to run the IUBMB Congress in
and discussions in the biochemical education space. Melbourne in 2024. Having people doing great jobs like
Encouraging the Society to increase its focus on this makes the role of the President infinitely easier!
biochemistry education has been on my agenda, and Finally, thank you all too as members – you of course
I am pleased that we have attracted an Education are the Society. See you all at the next meeting!
Plenary speaker for ComBio2022. Joel Mackay
President, ASBMB
PAGE 4 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020
ASBMB 2020 Meeting
With the postponement of ComBio2020 until 2022, ASBMB
hosted a virtual meeting in 2020. The ASBMB Council felt it
was important to provide our members with opportunities to
come together to maintain a sense community and celebrate
our award winners. We held an Education Symposium chaired
by Nirma Samarawickrema on 29 September and a Research
Symposium chaired by Tatiana Soares da Costa on 30 September.
Education Symposium
COVID-19 was the thunderbolt that hit our universities they experienced as a result of the sudden shift to remote
in 2020 and forced educators into remote teaching. learning, the strategies they used to adapt, and their
Biochemistry educators, like other educators worldwide, visions for a post-COVID learning environment. These
scrambled behind the scenes, urgently transforming their presentations were timely reminders to educators of the
teaching for online delivery while ensuring continuity, criticality of our ultimate audience – our students.
quality and integrity. This unexpected and rapid transition
to online remote learning resulted in the reinvention of
much of our teaching and learning, and the adoption
of a wealth of strategies and novel practices to engage
students in workshops, tutorials, practical classes and
assessment.
The ASBMB Education Symposium – Teaching
Remotely, Sharing Practice was held on 29 September
2020. The Education Symposium provided national
and international participants a platform to share their
insights and experiences, innovations and good practice Biochemistry students Ben Urzua and Rhianna Coscia.
to transform the student learning experience as we move
forward. The symposium had 250 registrants, with 131 from
This event offered a mix of short and extended across Australia representing all six states and a territory
presentations from educators who demonstrated how and 119 from overseas, many of whom were members of
they: the Federation of Asian and Oceanian Biochemists and
• Motivated students to learn online through game- Molecular Biologists (FAOBMB).
based platforms, digital portfolios, Zoom case-study ASBMB President, Professor Joel Mackay, attributed
workshops. the great level of participation in our event to the mutual
• Transformed large face-to-face lab classes to online commitment and drive of biochemistry educators to
laboratory classes without losing the interactivity enhance teaching practices and the value they place
of the face-to-face classes by using a variety of on educating and inspiring our future generations of
strategies including Zoom to guide a metabolomics scientists. This sentiment was echoed by Professor
computer practical, PYMOL and Sketchfab to map Roger Daly (Head, Biochemistry and Molecular Biology,
out and create guided tours of a protein. Monash University) in his welcome address.
• Developed skills such as evaluative judgement, The symposium showcased a snapshot of the innovations
research and writing skills through online implemented in remote learning. It is now up to the broader
approaches. education community to reflect upon, adapt and apply this
• Created authentic assessments even for large-scale learning as it is relevant to our specific student cohorts in
undergraduate research experiences, and created a post-COVID world. Professor Liz Johnson (Deputy Vice-
online assessments to avoid plagiarism through the Chancellor, Education, Deakin University) endorsed this
development of software that could generate unique idea in her keynote address, Online is the New Normal:
data sets. Teaching as We Work. “Disruption creates opportunity as
Contributions from our students were a highlight of the assumptions and conventions are challenged. It is time
conference. Third year student Benjamin Urzua (Monash to re-examine the value of each teaching mode and to
University) and second year student Rhianna Coscia select learning and assessment activities that leverage
(University of South Australia) discussed the challenges the strengths of online as well as face-to-face teaching.”
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 5
ASBMB 2020 Meeting
Keynote speaker Liz Johnson. Sophie Paquet-Fifield.
We congratulate the Education Symposium winners: We thank the ASBMB for supporting the vision of this
Best abstract (sponsored by Fisher Biotec Australia) inaugural online symposium, Fisher Biotec for sponsoring
Professor Gareth Denyer and Dr Alice Huang the best abstract award and Danielle Rika from the
University of Sydney Department of Biochemistry and Molecular Biology,
Generation of unique datasets to complement online Monash University, for her outstanding support to the
practicals and build student experimental design and Education Symposium Committee and her meticulous
troubleshooting skills attention to detail. As the ASBMB Education Symposium
Organising Committee, we gratefully acknowledge each
other and unanimously agree that we were a wonderful
team!
Our sincere thanks to our student participants, our
presenters who shared their practice and to all who
attended. The presentations highlight how educators rose
to the challenge of remote teaching.
Videos of the day’s presentations are available online.
ASBMB Education Symposium
Organising Committee
Gareth Denyer and Alice Huang. Nirma Samarawickrema, Monash University
Tracey Kuit, University of Wollongong
Highly Commended Abstract (sponsored by ASBMB) Amber Willems-Jones, University of Melbourne,
Dr Kathryn Jones and Dr Monica Kan Matthew Clemson, University of Sydney
University of Auckland, New Zealand Maurizio Costabile, University of South Australia
Creating interactive online biochemistry laboratories
using H5P
Kathryn Jones and Monica Kan.
Best Zoom Background (sponsored by ASBMB)
Dr Sophie Paquet-Fifield
University of Melbourne
For a background created collaboratively by her young
children and students
PAGE 6 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020
ASBMB 2020 Meeting
Research Symposium
On 30 September, we held a Research Symposium,
chaired by Tatiana Soares da Costa (ASBMB Editor
and Chair of Communications) with the help of State
Representatives: Benjamin Schulz, Erinna Lee, Kate
Brettingham-Moore, Kate Quinlan, Melissa Pitman and
Monika Murcha.
We had an exciting Research Symposium program
with two engaging plenary speakers. Professor Shelley
Berger (University of Pennsylvania) started her talk
discussing how epigenetic changes and pathways govern
social behaviour in ants and ended with how chromatin
enzymes modify the tumour suppressor p53. Professor National University) provided a great overview of the
Glenn King (University of Queensland) gave a fascinating protein work his lab does, with a focus on the evolution
talk on how a spider venom peptide can be used to treat of binding specificity in the amino acid binding proteins.
ischemic injuries of the heart and brain. Eppendorf Edman ECR Award winner Professor Si Ming
Man (Australian National University) discussed the role of
GBPs in inflammasome activation. We also had lightening
talks from ASBMB Travel Fellowship awardees, Dr Amy
Baxter (La Trobe University), Dr Steffi Cheung (University
of Melbourne), Dr Mengjie Hu (University of Melbourne)
and Anukriti Mathur (Australian National University).
The ASBMB AGM was held after lunch and with many of
our members attending, we had no issues with reaching
a quorum! Associate Professor Dominic Ng from the
University of Queensland was elected as ASBMB National
Secretary, taking over from Professor Briony Forbes,
who we thanked for her many years of hard work and
stewardship of the Society. The changing of the guard
continued as we welcomed new State Representatives
for ACT, NSW, QLD, TAS and VIC. At the conclusion of
the symposium, we had a happy hour using Spatial Chat,
which allowed us to ‘move around’ a crowd to join and
leave conversations, replicating as much as possible the
conference cocktail mixers we have sorely missed.
Research Symposium attendance numbers were
pleasing, with over 260 registrants from around Australia
and overseas. The two-day ASBMB meeting highlighted
the amazing advances our Australian biochemistry and
molecular biology community is making in education
and research. Thanks to the Organising Committee, the
Presentations by plenary speakers Shelley Berger and award sponsors and ASBMB President, Joel Mackay, for
Glenn King. their support.
Videos of the day’s presentations are available online.
We also heard from our 2020 ASBMB awardees. Planning continues for 2021, with an expanded East
Lemberg medallist Professor Trevor Lithgow (Monash Coast Protein Meeting (more details in the coming
University) described how porin loss leads to carbapenem months) and the FAOBMB Congress in Christchurch,
resistance in Klebsiella. SDR Scientific Education Award New Zealand. We look forward to seeing you then –
winner Dr Nirma Samarawickrema (Monash University) hopefully face-to-face!
presented recommendations for education amidst COVID Tatiana Soares da Costa
based on case studies. Boomerang Award winner Dr Chair, ASBMB 2020 Research Symposium
Matthew Doyle (National Institutes of Health Bethesda) La Trobe Institute for Molecular Science
discussed how BamA forms a translocation channel for La Trobe University
secretion of bacterial autotransporter proteins. Shimadzu T.SoaresdaCosta@latrobe.edu.au
Research medallist Professor Colin Jackson (Australian Twitter: @Tatiana_Biochem
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 7
PAGE 8 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020
Publications with Impact
Publications with Impact profiles recent, high impact publications by ASBMB members.
These short summaries showcase some of the latest research by presenting
the work in a brief but accessible manner. If your work has recently been
published in a high profile journal, please email editor@asbmb.org.au.
Unravelling the Speciation, Trafficking,
Autoinflammatory Potential of the Killer Protein, MLKL
Our team at the Walter and Eliza Hall Institute of Medical Research has published a trio of studies in
Nature Communications that shed new light on the protein, MLKL, and how it causes an inflammatory form
of cell death known as necroptosis. As outlined below, these studies use structural biology to understand
evolutionary changes in MLKL, advanced microscopy to visualise when and where MLKL is activated in
cells undergoing necroptosis, and genetic models to address how mutations in MLKL can trigger lethal
auto-inflammatory disease.
Davies KA, Fitzgibbon C, Young SN, Garnish SE, Yeung W, Coursier D, Birkinshaw RW,
Sandow JJ, Lehmann WIL, Liang LY, Lucet IS, Chalmers JD, Patrick WM, Kannan N, Petrie EJ,
Czabotar PE*, Murphy JM*. Distinct pseudokinase domain conformations underlie divergent
activation mechanisms among vertebrate MLKL orthologues. Nat Commun 2020;11:3060.
*Corresponding authors: czabotar@wehi.edu.au, jamesm@wehi.edu.au
As a pseudokinase,
MLKL is unable to catalyse
phosphotransfer reactions.
Instead, phosphorylation
of MLKL’s activation
loop by the upstream
kinase, RIPK3, is thought
to toggle a molecular
switch, such that the
killer N-terminal domain
becomes exposed and can
permeabilise the plasma
membrane to induce cell
death by necroptosis. The Crystal structures of the rat and horse MLKL pseudokinase domain, that were used to
underlying mechanism better understand species compatibility. PDB: 6VBZ, 6VC0.
was recently shown to
differ between mouse and human necroptosis, which between MLKL orthologues where they could seldom
led us to examine the extent of divergence among ‘talk’ to RIPK3 within mouse and human cells. Together,
vertebrate MLKL orthologues. By studying nine MLKL our findings suggest that the MLKL:RIPK3 cassette has
orthologues spanning multiple phylogenies, and solving rapidly co-evolved in different species, potentially due
the structures of the rat and horse MLKL pseudokinase to varying selection pressures exerted by the pathogens
domains, we identified a profound lack of compatibility that target each organism.
From left: André Samson,
Joanne Hildebrand and
Katherine Davies.
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 9
Publications with Impact
Samson AL*, Zhang Y, Geoghegan ND, Gavin XJ, Davies KA, Mlodzianoski MJ, Whitehead LW,
Frank D, Garnish SE, Fitzgibbon C, Hempel A, Young SN, Jacobsen AV, Cawthorne W, Petrie EJ,
Faux MC, Shield-Artin K, Lalaoui N, Hildebrand JM, Silke J, Rogers KL, Lessene G,
Hawkins ED*, Murphy JM*. MLKL trafficking and accumulation at the plasma membrane
control the kinetics and threshold for necroptosis. Nat Commun 2020;11:3151.
*Corresponding authors: samson.a@wehi.edu.au, hawkins.e@wehi.edu.au, jamesm@wehi.edu.au
MLKL normally resides in the cytoplasm, but during
necroptosis it translocates to membranes and kills cells
by disrupting plasma membrane integrity. In this study,
we used single-cell imaging to meticulously map the
activation and relocation of endogenous human MLKL
during necroptosis. We found that, once activated, MLKL
moves to the plasma membrane via Golgi-, tubulin- and
actin-dependent mechanisms, and that inhibiting these
trafficking mechanisms specifically slows the onset of
necroptotic cell death. Strikingly, during necroptosis,
MLKL co-trafficks with tight junction proteins – proteins
best known for their role in epithelial barrier formation.
This co-trafficking allows MLKL to accumulate into
micron-sized ‘hotpots’ at the plasma membrane during
necroptosis. In this work, we identified two new rate-
limiting checkpoints in necroptosis: (1) a trafficking Two cells undergoing necroptosis exemplifying the
checkpoint that controls the movement of MLKL to junctional accumulation of human MLKL.
the cell periphery, and (2) a junctional checkpoint
that renders necroptosis ‘contagious’ and dictates the
amount of MLKL needed at the plasma membrane to
trigger cell death.
Hildebrand JM*, Kauppi M, Majewski IJ, Liu Z, Cox AJ, Miyake S, et al., Murphy JM,
Alexander WS*, Silke J*. A missense mutation in the MLKL brace region promotes
lethal neonatal inflammation and hematopoietic dysfunction. Nat Commun 2020;11:3150.
*Corresponding authors: jhildebrand@wehi.edu.au, alexandw@wehi.edu.au, silke@wehi.edu.au
The signalling pathway that culminates in MLKL MLKL point mutant mouse strain (MlklD139V) in an ENU
activation and killer activity has many entry and branch mutagenesis screen long before MLKL was implicated
points, making it tough to tease apart the precise role of in necroptosis, where homozygous pups died soon after
MLKL-mediated cell lysis in the aetiology of inflammation birth. Our team found that this point mutation conferred
and disease. Serendipitously, our team identified a both constitutive activity to MLKL at the molecular level,
but that this deadly activity was very efficiently ‘kept in
check’ at the cellular level through MLKL proteolysis
below a threshold. This threshold is overwhelmed only
when two MlklD139V alleles are inherited, and only after
birth – physiologically manifesting as inflammation in/
around the lower head and mediastinum (salivary
glands, heart and thymus). We are excited to continue
exploring the inflammatory role of a very closely situated
cluster of human MLKL mutations which are present in
An activating mutation in mouse MLKL manifests in a up to 8% of individuals globally, and enriched (in trans)
deadly postnatal inflammatory syndrome. Longitudinal in a form of paediatric bone disease, CRMO.
section of 2-day old mouse mediastinum.
Katherine Davies, André Samson,
Joanne Hildebrand and James Murphy
Walter and Eliza Hall Institute of Medical Research
Department of Medical Biology, University of Melbourne
PAGE 10 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020Publications with Impact
Fluid Coupling in the Rotary Motor of Life
Sobti M, Walshe JL, Wu D, Ishmukhametov R, Zeng YC, Robinson CV, Berry RM, Stewart AG*.
Cryo-EM structures provide insight into how E. coli F1Fo ATP synthase
accommodates symmetry mismatch. Nat Commun 2020;11:2615.
*Corresponding author: a.stewart@victorchang.edu.au
F1Fo ATP synthase is a complex macromolecular
machine consisting of two coupled rotary motors:
the soluble F1 ATPase and the transmembrane
Fo motor. The F1 ATPase is a chemical motor
that synthesises adenosine triphosphate (ATP),
whereas the Fo motor is an electric motor powered
by proton flow. Together these motors make a major
contribution to the generation of cellular chemical
energy by converting the proton motive force (pmf)
into ATP, the universal cellular energy currency.
By imaging the intact enzyme from Escherichia
coli using cryo-electron microscopy (cryo-EM), the
Stewart lab and their collaborators were able to
generate detailed atomic-level information on how
energy is transferred elastically between the two The Stewart laboratory, from left: James Walshe, Yi Zeng,
motors. Alastair Stewart and Meghna Sobti.
Recent improvements in cryo-EM have produced
new insight on F1Fo ATP synthase, providing detailed resides in the membrane and is comprised of a ring of
information about how this enzyme functions at the c-subunits (the c-ring) that can rotate relative to a stator,
atomic level. Bacterial F1Fo ATP synthase has been the a-subunit. The motor is driven by the pmf, generated
studied for many decades and has been used as a model by oxidative phosphorylation or photophosphorylation,
system to understand ATP synthase function. The F1 and acts like a horizontal water wheel, with protons
ATPase is comprised of a hexameric ring of alternating sequentially binding to the c-ring from the periplasm
a- and b-subunits, with a single g subunit bound and rotating through it before being released into the
asymmetrically in the ring centre. As this central ‘rotor’ cytoplasm. The rotation of the c-ring is transferred to the
g-subunit rotates, it generates conformational changes central rotor (g subunit), thereby coupling the rotation of
in the a- and b- subunits. The F1 ATPase enzyme one motor to the other. An interesting feature of almost
operates with a binding-change mechanism, whereby all ATP synthases is a symmetry mismatch between the
rotation of the central rotor induces sequential binding F1 and Fo motors because the F1 ATPase has threefold
of ADP and inorganic phosphate in the b-subunits, rotational symmetry, whereas the Fo motor has tenfold
which are then combined to make ATP. The Fo motor symmetry (in E. coli). This mismatch causes a non-
The cryo-EM structure of
E. coli F1Fo ATP synthase.
a. Sorting of the particles
using 3D classification
resulted in nine discrete
sub-states.
b. The sub-states show
rotational ‘sub-stepping’
in the Fo motor, which is
mediated by a flexible
peripheral stalk.
c. Local resolution of
the F1 ATPase and
composition of the
catalytic sites.
d. Lipids (wheat density)
bridge protein subunits
in the Fo motor.
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 11Publications with Impact
integral H+/ATP ratio and consequently, the motors need store elastic energy in the ‘peripheral’ stalk to overcome
to be coupled elastically to operate efficiently. the symmetry mismatch between the two motors (b).
High resolution cryo-EM maps of the intact E. coli F1Fo High resolution information in the catalytic domain also
ATP synthase were generated by imaging the detergent- gave insight into how the F1 ATPase is inhibited from
solubilised complex in the presence of MgADP. These operating in reverse (c), and maps focussing on just the
maps highlighted nine different sub-states that described Fo motor showed a novel lipid interaction that can bridge
the molecular motion of the complex, nucleotide binding a subunit within the c-ring with the stator a subunit (d),
occupancy, and lipid-mediated interactions (see figure). thereby increasing the interaction surface which may
Of greatest interest was the ‘sub-stepping’ observed in aid fluid coupling.
the Fo motor, which showed how the transmembrane Alastair Stewart
motor can rotate independently of the F1 ATPase and Victor Chang Cardiac Research Institute
The Natural Function of a
Multidrug Resistance Transporter
Shafik SH, Cobbold SA, Barkat K, Richards SN, Lancaster NS, Llinás M, Hogg SJ,
Summers RL, McConville MJ, Martin RE*. The natural function of the malaria
parasite’s chloroquine resistance transporter. Nat Commun 2020;11:3922.
*Corresponding author: rowena.martin@anu.edu.au
“What is the natural function of the Plasmodium as a drug target. In this study, the Martin lab and
falciparum chloroquine resistance transporter collaborators at the University of Melbourne and
(PfCRT)?” has been a major unanswered question the Pennsylvania State University provide the long-
in malaria parasite biology for two decades. awaited elucidation of PfCRT’s native substrates
Mutations in PfCRT were originally identified as and normal physiological role. PfCRT functions
the main cause of chloroquine resistance in P. to export host-derived peptides containing four to
falciparum, but are now known to play a key role eleven residues from the digestive vacuole to the
in multidrug resistance. The transporter resides at cytosol, thereby providing a source of amino acids
the membrane of the parasite’s digestive vacuole for parasite metabolism and preventing the osmotic
– a lysosomal-type organelle in which many stress of this organelle.
antimalarial drugs accumulate, act, and/or are The malaria parasite consumes vast quantities of host
activated. Mutant isoforms of PfCRT contribute proteins (mainly haemoglobin) to provide the space and
to multidrug resistance primarily by transporting amino acids it requires for proliferation within the host
drugs out the vacuole. PfCRT is also essential erythrocyte, and also to maintain the osmotic balance
for parasite survival and has itself been identified of the parasitised cell. This process occurs within the
Wildtype (wt) PfCRT
exports peptides from
the digestive vacuole
into the parasite cytosol.
The diminished capacity
of the drug resistance
conferring isoform (mut)
for peptide transport
causes a build-up of
peptides and amino
acids, thereby raising
the vacuole’s osmotic
pressure and reducing
the rate of digestion.
PAGE 12 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020Publications with Impact
eleven residues, varying in both charge and composition,
are substrates of PfCRT in vitro and in situ. Furthermore,
we showed that the protein does not transport other
metabolites and/or organic or inorganic ions. The
transport of peptides and peptide mimics via PfCRT is
saturable, can be blocked by known PfCRT inhibitors
Sarah (e.g. verapamil), and is dependent on protons as well as
Shafik on a second solute that remains to be identified, but which
(left) and is naturally present in the Xenopus oocyte. Relative to
Rowena wildtype PfCRT, the drug resistance conferring isoforms
Martin. exhibit reduced rates of peptide transport and accept
a narrower range of peptides and peptide mimics. The
acidic environment of the parasite’s digestive vacuole. reduced capacity of mutant PfCRT to efflux peptides
Importantly, alterations to PfCRT can affect the normal out of the vacuole accounts for the accumulation of
physiology of this organelle as well as the growth of the these substrate peptides in the drug resistant lines, and
parasite. For example, downregulation of PfCRT causes explains the impaired fitness of parasites expressing
the vacuole to swell and impairs parasite growth, and mutant isoforms of the transporter. The physiological
potent inhibition of mutant PfCRT results in parasite relevance of this correlation was further substantiated
death. Moreover, the mutant isoforms that confer drug when we used the peptidomic datasets to correctly
resistance typically impose a fitness cost upon the predict host-derived peptides as being substrates or
parasite, the severity of which is dependent upon the non-substrates of PfCRT. Our work indicates that the
number and nature of the mutations. PfCRT-mediated transport of peptides from the vacuole
Attempts to use heterologous expression systems to to the cytosol serves to (1) provide a source of amino
identify the native substrates of PfCRT in vitro have acids to support the parasite’s high growth rate, and (2)
produced wildly different ‘natural functions’ for the reduce peptide levels within the vacuole and thereby
protein, with there being no convincing support for prevent the osmotic stress, swelling, and dysfunction
one claim over the others. We employed the Xenopus of this organelle. The resolution of PfCRT’s native
oocyte expression system, as well as measurements substrate-specificity and physiological role provides a
of solute transport, drug activity, and metabolite levels foundation for the development of drugs that target both
in isogenic parasite lines expressing different pfcrt its normal and drug resistance conferring functions.
isoforms, to identify, and independently validate, the Rowena Martin
natural substrates of PfCRT. Research School of Biology
Our work revealed that host-derived peptides of four to Australian National University
Uncovering a New Way in Which Tumours Co-opt Their
Microenvironments to Promote Disease Progression
Boyle ST, Poltavets V, Kular J, Pyne NT, Sandow JJ, Lewis AC, Murphy KJ, Kolesnikoff N,
Moretti PAB, Tea MN, Tergaonkar V, Timpson P, Pitson SM, Webb AI, Whitfield RJ, Lopez AF,
Kochetkova M*, Samuel MS*. ROCK-mediated selective activation of PERK signalling
causes fibroblast reprogramming and tumour progression through a
CRELD2-dependent mechanism. Nat Cell Biol 2020 22(7):882–895.
*Corresponding authors: marina.kochetkova@unisa.edu.au, michael.samuel@unisa.edu.au
Cancer-associated fibroblasts (CAFs) have been Rho-ROCK pathway with the tumour secretome
reported to exhibit context-dependent tumour- while revealing a novel tumour-promoting role for
promoting or tumour-suppressing capacities. PERK signalling and the enigmatic EGF domain-
However, the mechanisms underpinning these containing protein CRELD2.
contexts are not precisely defined. In collaboration Cancer cells need to modify and remodel the
with other researchers at the Centre for Cancer environments within which they arise in order to facilitate
Biology, the Walter and Eliza Hall Institute of Medical their survival, and to enhance their growth and spread.
Research, the Garvan Institute of Medical Research This is because the normal tissue microenvironment
and the A*STAR Institute of Molecular Cell Biology, is hostile to the survival and persistence of abnormal
the Samuel lab at the Centre for Cancer Biology cells. To establish a permissive environment, cancer
has defined a novel signalling axis connecting the cells therefore need to influence the behaviour of their
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 13Publications with Impact
Exposure to Creld2
enhances the
capacity of cancer-
associated fibroblasts
to promote tumour
progression when
they are orthotopically
co-engrafted with
primary mammary
tumour cells into
immune-competent
hosts. Creld2 is
secreted by tumour
cells in which ROCK is
activated, via a novel
mechanism by which
the PERK-regulated arm
of the unfolded protein
response is specifically
engaged in the absence
of ER-stress.
genetically normal microenvironment. Herein lies a key ECM, the bulk of the tumour ECM is secreted by cells
vulnerability. Since cancer cells need to persistently populating the microenvironment, such as fibroblasts
maintain their influence over normal cells, interfering and some immune cells.
with the signals passing between cancer cells and the To test the hypothesis that cancer cells influence
microenvironment may provide us with opportunities to the behaviour of fibroblasts via secreted factors, we
normalise the microenvironment such that it is no longer exposed primary mammary tumour fibroblasts from the
a permissive one. MMTV-PyMT model of mammary cancer to medium
We had previously demonstrated that the Rho-ROCK conditioned either by primary mammary tumour cells
signalling pathway, which is frequently activated in in which the ROCK pathway was activated via the
epithelial cancers, lies upstream of key changes expression of a construct encoding conditionally active
within the microenvironment. In particular, tumours in ROCK, or control cells containing a version of the same
which this pathway was activated had high levels of construct encoding kinase-dead ROCK. Fibroblasts
collagen and other extracellular matrix (ECM) proteins, exposed to medium conditioned by tumour cells in
enhancing their mechanical stiffness. Elevated tissue which ROCK had been activated exhibited induction of
stiffness is strongly associated with disease progression, genes encoding ECM proteins and markers associated
perpetuated by mechano-transduction signalling in with tumour-promoting CAFs. These fibroblasts were
tumour cells that are located within stiff tissues. These also more motile than control fibroblasts and cell-
signalling pathways, including signalling via YAP/ derived matrix prepared from them elicited collective
TAZ, beta-catenin and FAK, regulate key processes and organised migration in tumour cells. Fibroblasts that
that facilitate tumour cell survival, proliferation and had been exposed to medium conditioned by primary
migration. However, a key question raised by these mammary tumour cells, in which ROCK was activated,
observations was how Rho-ROCK signalling within enhanced the growth of tumours when co-engrafted with
tumour cells resulted in the production of large amounts primary PyMT tumour cells into the mammary fat pads
of ECM proteins. While tumour cells do indeed produce of wildtype, immune-competent FVB/n female mice.
PAGE 14 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020Publications with Impact
To identify the secreted factors that may be responsible (ER)-stress. Surprisingly but satisfyingly, recombinant
for inducing the tumour-promoting characteristics in Creld2 was able to recapitulate the effect of ROCK-
mammary tumour fibroblasts, we conducted proteomic conditioned medium on mammary tumour fibroblasts,
analysis of the secretome of primary PyMT mammary rendering them tumour-promoting.
tumour cells in which ROCK had been activated, and Analysis of signalling downstream of ROCK revealed
compared this with the secretome of primary PyMT that cells in which ROCK was activated exhibited
mammary tumour cells expressing kinase-dead ROCK. phosphorylation and activation of Perk, a key sensor
Among the differentially secreted proteins was Creld2, of ER-stress in one arm of the unfolded protein
a relatively obscure protein that was known to be response, and indeed that signalling downstream of
secreted by cells subjected to endoplasmic reticulum Perk was engaged in these cells. Signalling through
Perk increased the levels and nuclear translocation of
the transcription factor Atf4, which we demonstrated
to transcriptionally regulate the gene encoding Creld2.
This explained the increased production of Creld2 by
cells in which ROCK was activated.
Inducing ER-stress in cancers to precipitate UPR-
mediated immunogenic cell death is an approach that
is currently the focus of translational research as a
cancer therapy. Our work therefore serves as a timely
warning that this approach may yield the unintended
consequence of enhancing tumour progression via the
generation of tumour-promoting CAFs.
Sarah Boyle, Marina Kochetkova and
Michael Samuel, Centre for Cancer Biology
SA Pathology and University of South Australia
Sarah Boyle, Marina Kochetkova and Michael Samuel.
Mutational Landscape of Gall Bladder Cancers
Pandey A*#, Stawiski EW*#, Durinck S#, Gowda H#, Goldstein LD, Barbhuiya MA, Schroder M,
Sreenivasamurthy SK, Kim S, Phalke S, Suryamohan K, Lee K, Chakraborty P, Kode V, Shi X,
Chatterjee A, Datta K, Khan AA, Subbannayya T, Wang J, Chaudhuri S, Gupta S, Srivastav BR,
Jaiswal BS, Poojary SS, Bhunia S, Garcia P, Bizama C, Rosa L, Kwon W, Kim H, Han Y, Yadav TD,
Ramprasad VL, Chaudhuri A, Modrusan Z, Roa JC, Tiwari PK, Jang J-Y*, Seshagiri S*.
Integrated genomic analysis reveals mutated ELF3 as a potential
gallbladder cancer vaccine candidate. Nat Commun 2020;11:4225.
*Corresponding authors: pandey.akhilesh@mayo.edu,
eric.s@medgenome.com, jangjy4@snu.ac.kr, sekar@sgrf.org
Gall bladder cancer (GBC) is an aggressive characterise genomic alterations associated with
gastrointestinal malignancy with a poor prognosis. GBC. A total of 167 GBC samples and 39 gall bladder
GBC incidence rates are particularly high in specific non-neoplastic lesions with corresponding matched
geographic regions of the world including Chile, normal tissue were sequenced. This enabled us to
Bolivia, Peru, Korea, Japan and India. Reasons for identify genomic alterations frequently observed in
higher incidence rates in these regions remains GBC and determine if there were differences among
unclear. Women are two to six times more at risk of tumors from different geographic regions.
GBC than men. The median survival of patients with We identified several significantly mutated genes
GBC is generally less than a year. This is mainly that were not previously linked to GBC. This included
because GBC patients are diagnosed at an advanced ELF3, a frequently mutated gene in GBC with genomic
stage of the disease. Cholelithiasis and cholecystitis alterations in 21% of tumors. We integrated somatic
are some of the well-known risk factors of GBC. mutation, copy number variation and gene fusion data to
We established an international collaboration identify affected pathways in GBC. TP53/RB1 pathway
between researchers from India, USA, South Korea was most commonly altered in GBC. We also observed
and Chile, and performed whole genome, exome WNT pathway and KEAP1/NFE2L2 pathway activation
and transcriptome sequencing to identify and in GBC. Activating mutations in CTNNB1 and RSPO3
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 15Publications with Impact
fusion were primary drivers of WNT pathway activation.
We found inactivating mutations in SWI/SNF pathway
genes including SMARCA4, ARID1A and ARID2. We
also identified therapeutically actionable mutations in
RAS/PI3K pathway involving frequent alterations in
ERBB2, ERBB3, BRAF and PIK3CA. About 20% of all
tumors sequenced in our study had actionable mutations
based on approved therapies catalogued in OncoKB.
Immunotherapy has revolutionised cancer treatment.
Significant survival benefits have been observed
in various cancers including melanoma and lung
cancer. For the first time, we report GBC patients with
mismatch repair defects who have characteristic high
mutation burden and are candidates for check-point
immunotherapy. To further determine the presence of
cancer neoantigens that can be used either alone or in
Significantly mutated genes in gall bladder cancer.
combination with check-point inhibitors, we evaluated
non-synonymous somatic mutations as candidate the potential to use cancer immunotherapy for treating
neoantigens. Our analysis identified an average of 15 GBC. Beside serving as a resource for further studying
neoantigens/tumor that were predicted to have high- GBC and developing therapies, our dataset identified
affinity for MHC class I. Most predicted neoantigens many actionable GBC alterations that can be treated
were derived from frequently mutated genes such as using approved therapies.
TP53, ELF3, CTNNB1, ERBB2, ARID1A and CDKN2A. Harsha Gowda
Using peripheral blood mononuclear cells from HLA- QIMR Berghofer Medical Research Institute
matched healthy donors, we determined the ability of
mutant peptides to activate T-cells. Mutant peptides from
ELF3, ERBB2 and TP53 were found to activate T-cells Left:
suggesting that these peptides are potential cancer Harsha
vaccine candidates. Some of the ELF3 neoantigens can Gowda.
be used as a common cancer vaccine candidate as they
are recurrent mutations in GBC and other cancers such Right:
as colon cancer and ampullary carcinomas. Somasekar
Our comprehensive study identifies for the first time Seshagiri.
Structural Venomics: from Single to
Double Knots and Everything in Between
Pineda SS#*, Chin YKY#, Undheim EAB, Senff S, Mobli M, Dauly C, Escoubas P,
Nicholson GM, Kass Q, Guo S, Herzig V, Mattick JS, King GF*. Structural venomics reveals
evolution of a complex venom by duplication and diversification of an ancient
peptide-encoding gene. Proc Natl Acad Sci USA 2020;117(21):11399–11408.
#Equal first authors
*Corresponding authors: glenn.king@imb.uq.edu.au, sandy.spineda@gmail.com
Spiders and other venomous animals depend on underpinnings of venom complexity. We found that
the production of complex venoms for defence, the venom of the Australian funnel-web spiders
prey capture and competitor deterrence. Most evolved primarily by duplication and structural
spider venoms are dominated by disulfide-rich elaboration a single ancestral knottin gene.
peptides with molecular masses of 3–8 kDa. Spiders evolved from an arachnid ancestor around
However, the mechanisms employed by spiders to 450 million years ago (1). Currently, there are more than
generate such chemically and pharmacologically 100,000 extant species of spiders, making them one
diverse venom cocktails is not well understood. of the most successful animal lineages on the planet.
To address this question, we combined omics and Like other venomous invertebrates, spiders rely on their
structural biology techniques, a new approach that venom to capture prey and defend themselves against
we coined ‘structural venomics’, to investigate the predators. The ongoing battle between venomous
PAGE 16 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020Publications with Impact
Structural innovations in spider venoms knottins. Overview of
toxin and protein superfamilies highlighting the main mechanisms
by which toxins have been duplicated, conjugated and
elaborated upon to form the diversity of knottin scaffolds found
in venom of the Australian funnel-web spider H. infensa. In all
structures, disulfide bonds are shown as red tubes, b-sheets and
a-helices are highlighted in blue and green, respectively.
Insert: Structural alignment of the core knottin regions of DRPs
from superfamilies 1 (green), 6 (purple), 17 (pink), 22 (yellow)
and 23 (orange), highlighting conservation of the knottin motif
(disulfide-directed b-hairpin in the case of 22) and irrespective of
the elaborations outside the core region.
animals and their prey and predators places a constant
selection pressure on venom efficacy, and over millions
of years this has resulted in complex arsenals of venom
compounds that vary in size and pharmacological
activity. Spider venoms are dominated by ‘short’ (2–5
kDa) and ‘long’ (6–9 kDa) disulfide-rich peptides
(DRPs). Most spider-venom DRP structures solved to
date correspond to ‘short’ peptides that contain a knottin
motif in which three disulfide bonds are arranged in a
pseudo-knot configuration.
The venom of the Australian funnel-web spider
Hadronyche infensa is one of the most complex
chemical arsenals in the natural world, comprising
>3000 peptide toxins. We used a combined proteomic,
transcriptomic and structural biology approach to
explore the mechanism by which these spiders evolved
such complex toxin repertoires. We showed that H.
infensa produces 33 superfamilies of venom peptides From left: Sandy Pineda, Yanni Chin and Glenn King.
and proteins, and that 26 these superfamilies are
DRPs. Moreover, 15 of these DRPs contribute to >90%
of the venom proteome. Structure elucidation using Sandy Pineda
NMR spectroscopy revealed that most of the DRPs Institute for Molecular Bioscience
are structurally related but present a range of structural University of Queensland
innovations. The structural diversity ranged from DRPs Current affilitation:
with a simple knottin motif to highly elaborated knottin Brain and Mind Centre
domains and double-knot domains. Remarkably, this University of Sydney
work enabled us to conclude that the incredible diversity Reference
of DRPs in the venom of Australian funnel-web spiders 1. Lozano-Fernadez J, et al. (2016) Philos Trans R Soc
is largely derived from a single ancestral knottin gene. Lond B Biol Sci 371:20150133.
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AUSTRALIAN BIOCHEMIST | NO
VOL 51 +613 2DECEMBER
9541 3500
2020ASBMB Education Feature
The ASBMB Education Feature is coordinated by Nirma Samarawickrema
(nirma.samarawickrema@monash.edu) and Tracey Kuit (tracey_kuit@uow.edu.au).
Online Lessons from Our Students –
2020 ASBMB Education Symposium
Tracey Kuit (University of Wollongong) and Amber Willems-Jones
(University of Melbourne) interview undergraduate
Biochemistry students Benjamin Urzua and Rhianna Coscia
At the recent 2020 ASBMB Education Symposium, connected and up-to-date was an important adaptation,
a student panel was held with two undergraduate as was talking to my friends for encouragement. This
students: Benjamin Urzua, a third year Bachelor of helped to put everything in perspective and helped me
Science/Bachelor of Arts student at Monash University to persevere.
and Rhianna Coscia, a second year Bachelor of Medical Rhianna – Generally, I adapted well to the transition
Science student at the University of South Australia. online. A strategy I utilised was to stick to my timetable
Rhianna and Ben shared their experiences learning as if teaching were on campus. This allowed me to keep
biochemistry online in 2020. Responses to questions up-to-date with lectures and have tutorial answers ready
have been paraphrased and condensed with permission. to go for the tutorial Zoom session. The early release
of lecture recordings was really valuable as I could get
ahead in my study, allowing ample time for content
revision at the end of semester.
What helped you keep engaged online?
Ben – Online Q&A Zoom sessions after a set of lectures
Biochemistry were very useful to clarify understanding. Having
students Ben small group online breakout rooms during the tutorial
Urzua (left) and sessions, then coming back to the main large group to
Rhianna Coscia. share our answers. Fresh lectures, rather than the use
of pre-recorded lectures from previous years, were more
engaging. Online laboratories remained one of the most
What were the challenges or difficulties with the engaging aspects of online learning.
rapid move to online learning in 2020? Rhianna – I appreciated the recording of classes
Ben – My main difficulties were keeping to a schedule, delivered online. Whilst I joined classes live, recordings
maintaining a sense of reality and having a sense of allowed access at any time, and assisted revision.
accomplishment. It was challenging not having the Though, seeing my tutors or lecturers’ faces whilst
chance to interact with other students, though small they conveyed the information on Zoom really assisted
group breakout rooms online were the most useful tool in keeping me engaged, as seeing hand gestures and
to overcome this problem of reduced student interaction. models provided a human element to what was a very
Rhianna – Challenges included ensuring my home was technologically driven environment.
suitably set up for a home study environment, quiet and
with reliable internet. An unexpected challenge was the What were the unexpected benefits of online
difficulty of taking a break from online studies. With all practical classes?
events cancelled, I found myself spending extended Ben – Unexpectedly, the practical classes were the
periods of time on university work without a break. As favourite part of my units. They encouraged me to become
online learning continued, I overcame this by taking a more active learner in the process and to understand the
regular breaks throughout my day. I felt more focussed protocols, why each reagent was important and to simply
after incorporating this. be more curious. An online quiz prior to the start of the
lab ensured we understood the different techniques we
How did you adapt to learning online? were going ‘to do’. During the lab, we would go through
Ben – I adapted quite well, though it wasn’t until the each protocol step while we were asked questions. At
last period of the first semester that I felt that what I had the end of each session, we had a quiz to complete. This
accomplished so far was due to my own merit. Staying unexpected benefit in deeper learning may have been
VOL 51 NO 3 DECEMBER 2020 AUSTRALIAN BIOCHEMIST PAGE 19ASBMB Education Feature
because we had more time to focus on what we were Zoom sessions/forums to allow the social interaction and
doing as opposed to rushing to finish everything during a networking of students, separate to direct class work,
traditional laboratory session. may also assist the online university experience.
Rhianna – Moving practical classes online was naturally
very disappointing, because undertaking a science What are your recommendations for educators?
degree, the practical, hands on skills are very transferable Ben – Combining an educational format of self-taught/
to the workplace. However, the transition of practical self-paced online activities with face-to-face or online
classes to the online environment was successful. We discussions, where students are encouraged to
had a range of online materials and interactive activities come prepared with the lecture content and have the
which substituted the face-to-face practicals. This opportunity to go beyond it. Secondly, having activities
included practical videos which allowed us to visualise in which students depend on the participation of other
what we would have been doing in the practical session, students, e.g. there could be some group activities where
but also provided greater understanding to how supplied each student needs to contribute something by having
sample results were obtained from recipe-like steps in a completed a task prior to the lecture/tutorial. This could
lab book. help students to become more active learners and to
collaborate.
What were your frustrations with online learning? Rhianna – Continuing to offer online interactive activities
Ben – I understand that collusion can be an issue and to supplement face-to-face learning, as it provides
that having your notes by your side is an impediment instantaneous feedback about content understanding,
to reliably measure how students are able to apply the and allows access at time of need. Secondly, consider
unit’s content. However, sometimes test time constraints communication between teaching staff and students a
meant we didn’t have enough time to show our true key importance when delivering learning online. There
potential. Additionally, it was frustrating not being able to have been occasions in some classes where we have
draw reaction mechanisms or biochemical pathways. not been contacted by educators, leaving students in
Rhianna – Rather than a frustration as such, the limbo about what to do, what time to log on etc., causing
reliability of the online assessment platform was anxiety undue stress. Thirdly, adhere to the timetable, utilising
inducing. For example, in one particular test, my internet visual elements and interactive activities (e.g. Kahoot) to
connection dropped out due to the number of students maintain the focus of students who are at home.
logging on simultaneously. This caused additional anxiety
in a test setting. There are technological aspects of online
learning (i.e. countdown time limits, file compatibility,
etc.) that can occasionally be unreliable. Tracey Kuit is an Education-
Focused Associate Professor
What things would you change? in the School of Chemistry
Ben – Having more instances for students to engage and Molecular Bioscience,
with one another. For example, providing online readings University of Wollongong.
or short videos related to lectures and giving students tracey_kuit@uow.edu.au
a chance to discuss with the lecturer and develop their
critical thinking skills. I would be cautious, however, not
to expect too much from students, because sometimes
it felt that because students were at home, academics
assumed they had more time and therefore gave an Dr Amber Willems-Jones
increased workload as a result. is a Senior Lecturer in the
Rhianna – As someone that likes to be organised and get Department of Biochemistry
ahead in my studies, I value the upload of content early and Molecular Biology,
to have efficient revision time at the end of semester. University of Melbourne.
Online discussion forums also permit students to interact amber.willems@unimelb.edu.au
with one another about content-related questions. Some
PAGE 20 AUSTRALIAN BIOCHEMIST VOL 51 NO 3 DECEMBER 2020You can also read
