Working towards diversity, equity and inclusion in the sciences

Bulbul ChakrabortyBulbul Chakraborty
Enid and Nate Ancell Professor of Physics
Division Head, Sciences, School of Arts and Sciences

This blog is addressed to my colleagues in the division of science. 

As scientists, we pride ourselves on solving problems, often ones that lead to paradigm shifts.  A challenge that we have all grappled with is how to cultivate and nurture a truly diverse community of scientists.  How do we create an environment that is inclusive and accessible to all that seek to enter the sciences and experience the invigorating practice of  science that  we live and breathe?  How do we open our doors and not be gatekeepers? 

I am writing this blog because the many conversations that I have had over this summer has convinced me that this is the right time for a concerted effort to push towards our objectives. As scientists we know that half the battle is going to the core of a problem, and representing it in a way that tells us what actions to take.   What I have become aware of is  that the anecdotal evidence on who leaves the sciences is being made quantitative and rigorous.  Words are being put to our experiences and structures are being offered that we can use to take actions.  We have colleagues at Brandeis and in the broader community of science educators that have thought long and hard about how to bring about change in STEM education. We can all learn from them.  

I am urging all of you to share resources that you are aware of that will help us create actionable goals and structural changes.  Towards that, here is a link to an organization called “SEA CHANGE”, within the auspices of the American Association for the Advancement of Science: https://seachange.aaas.org/.  In particular, they are hosting a series of Webinars under the banner “Talking about Leaving Revisited”: https://seachange.aaas.org/events  that I have registered for and I encourage you to do so if you can.

I intend to make this a monthly blog that reflects my thoughts on diversity, equity and inclusion in the sciences at Brandeis.

Susan Lovett elected to the American Academy of Arts and Sciences

Susan LovettSusan Lovett, the Abraham S. and Gertrude Burg Professor of Microbiology, has been elected to the American Academy of Arts and Sciences. She was among the 276 outstanding individuals that were elected to the Academy in 2020 and announced on April 23. Brandeis University Professor, Anita Hill, joins Professor Lovett as a 2020 member of AAAS.

The Lovett lab studies the fundamental mechanisms by which cells preserve genetic information by the study of DNA damage repair and mutation avoidance in the model organism Escherichia coli. Additionally, they research how cell cycle events including DNA replication and chromosome segregation are coupled to cellular physiology and to the status of the chromosome.

Lovett joins other Brandeis science faculty members: Jeff Gelles, Gina Turrigiano, James Haber, Michael Rosbash, Eve Marder, David Derosier, Gregory Petsko, Stanley Deser, and Edgar Brown, Jr.

Founded in 1780, the Academy recognizes the outstanding achievements of individuals in academia, the arts, business, government, and public affairs.

Read more: BrandeisNow

Autism-linked Gene Keeps Brains in Balance

Mutations in the human Shank3 gene – so called “Shankopathies” – are strongly associated with Autism-spectrum disorders and intellectual disability, and appear to increase risk for a number of other disorders such as bipolar disorder and epilepsy. How it is that loss of function of this single gene generates pervasive disfunction within the neural circuits that underlie cognition and behavior is not understood. Now a recent report from the Turrigiano lab at Brandeis (Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1. Neuron. 2020 Mar 10. ) sheds light into this process, by showing how Shank3 loss disables mechanisms that normally act to keep brain circuitry in balance. Much as your body maintains a constant temperature through the use of internal thermostats and negative feedback mechanisms, brain circuits maintain balanced activity – neither too low and unresponsive, nor too high and hyperactive – by using a set of so-called “homeostatic” plasticity mechanisms to keep circuit excitability within an ideal range. This process is especially important during childhood and adolescence, because developing circuits can easily get out of balance as brain circuitry changes as a result of normal developmental processes.

Using mouse and rat models of human Shankopathies, the team, led by Research Associate Vedakumar Tatavarty, found that loss of Shank3 disables these homeostatic plasticity mechanisms and prevents brain circuits from compensating for changes to sensory drive. These defects in homeostatic plasticity are due to acute loss of Shank3 within individual neurons, meaning they are not an indirect effect of messed-up circuit wiring caused by loss of the gene throughout development. This finding suggests that Shank3 is a fundamental part of the cellular machinery that normally mediates homeostatic plasticity. The team went on to show that homeostatic plasticity could be restored after Shank3 loss by treatment with Lithium – a drug with a long history of use to treat neuropsychiatric disorders such as bipolar disorder – and that Lithium was also able to reduce a repetitive grooming behavior in mice that lack Shank3. These mice normally groom to excess, even to the point of self-injury, but a week of lithium treatment was able to reduce grooming to normal levels.

So do these findings suggest that Lithium might be useful in treating human Shankopathies? While Lithium remains the frontline treatment for some human disorders such as bipolar disorder, it is not well-tolerated, says Turrigiano, “and of course we cannot extrapolate from findings in mice directly to humans. Instead, we hope to use Lithium as a tool to reveal the pathways that can restore homeostatic plasticity in Shankopathies, which in the long term may allow us to design better, more specific interventions”. Defects in homeostatic plasticity have been implicated in a wide range of human brain disorders ranging from Autism spectrum disorders to Alzheimer’s disease, so these studies are likely to have important implications for overall brain health.

Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1. Tatavarty V, Torrado Pacheco A, Groves Kuhnle C, Lin H, Koundinya P, Miska NJ, Hengen KB, Wagner FF, Van Hooser SD, Turrigiano GG. Neuron. 2020 Mar 10. pii: S0896-6273(20)30184-7. doi: 10.1016/j.neuron.2020.02.033.

SPROUT and I-Corps Applications are Open

Sprout logoThe Brandeis Innovation SPROUT and I-Corps programs offer support for bench and non-bench research. Both programs offer funding in different amounts, mentorship, training and help in further exploring the commercial potential of inventions. SPROUT supports bench research, while I-Corps emphasizes training for both bench and non-bench researchers in developing the commercial potential of discoveries, with small grants and extensive training programs. You can apply to one or both programs.

  • If you have a technology / solution that you have started developing and you would like to get funding for it via SPROUT and/or I-Corps, then please complete this form
  • If you do not already have a technology, then you can complete this form to qualify for the I-Corps training program and be matched with a team

Icorps logo

SPROUT teams will get the chance to qualify for up to $30,000 in funding. The I-Corps program provides entrepreneurial training and covers the core of commercializing a technology or building a startup. It comes with an NSF $750 travel and training stipend and an NSF I-Corps certificate/digital badge.

Apply by February 25, 2020 at 11:59PM

Cooling Mosquitoes’ Drive for Human Blood

Drawing from Smithsonian Magazine depicting mmosquitoes and thermonter

Anopheles gambiae mosquitoes use a receptor called IR21a to navigate toward warmth, a cue that signals they’re near food (Crystal Zhu, Garrity Lab, Brandeis University).

In a recent Science paper, the Garrity lab reported that they have found an important step in how mosquitoes sense human warmth. Once found, human blood becomes a food source for the insects’ eggs. Unfortunately,  mosquito bites have, over the centuries, spread disease and misery among humans.

The lab genetically modified mosquitoes to stop expressing a molecular thermostat called IR21a in their antennae. This reduced the insects’ ability to find the heat generated by humans. The hope is that this discovery will help remove the mosquitoes temperature sensors so they don’t spread disease. This discovery has also been summarized in the Smithsonian Magazine.

Paper: Mosquito heat seeking is driven by an ancestral cooling receptor. Chloe Greppi, Willem J. Laursen, Gonzalo Budelli, Elaine C. Chang, Abigail M. Daniels, Lena van Giesen, Andrea L. Smidler, Flaminia Catteruccia, Paul A. Garrity. Science  07 Feb 2020: Vol. 367, Issue 6478, pp. 681-684.

 

 

Goode, Gelles and Kondev labs synergize in discovery of a new synergistic actin depolymerization mechanism

Shashank Shekhar, Jane Kondev, Jeff Gelles and Bruce Goode

Shashank Shekhar, Jane Kondev, Jeff Gelles and Bruce Goode

All animal and plant cells contain a highly elaborate system of filamentous protein polymers called the actin cytoskeleton, a scaffold that can be rapidly transformed to alter a cell’s shape and function. A critical step in reconfiguring this scaffold is the rapid disassembly (or turnover) of the actin filaments. But how is this achieved? It has long been known that the protein Cofilin plays a central role in this process, but it has been unclear how Cofilin achieves this feat. Cofilin can sever actin filaments into smaller fragments to promote their disassembly, but whether it also catalyzes subunit dissociation from filament ends has remained uncertain and controversial. Until now, this problem has been difficult to address because of limitations in directly observing Cofilin’s biochemical effects at filament ends. However, a new study published in Nature Communications led by postdoctoral associate Dr. Shashank Shekhar, jointly mentored by Bruce Goode, Jeff Gelles and Jane Kondev, uses microfluidics-assisted single molecule TIRF imaging to tackle the problem.

The new study shows that Cofilin and one other protein (Srv2/CAP) intimately collaborate at one end of the actin filament to accelerate subunit dissociation by over 300-fold! These are the fastest rates of actin depolymerization ever observed. Further, these results establish a new paradigm in which a protein that decorates filament sides (Cofilin) works in concert with a protein that binds to filament ends (Srv2/CAP) to produce an activity that is orders of magnitude stronger than the that of either protein alone.

Video of cofilin and Srv2/CAP collaborating

The work was funded by National Institutes of Health, National Science Foundation MRSEC and Simons Foundation grant.

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