HackMyPhD to be held Thursday, July 26

HackMyPhD is Brandeis’ annual event to showcase the latest opportunities available to science, math, and applied arts graduate students. Students will be exposed to a variety of educational and professional opportunities for growth through funding, networking, and internship and job opportunities.

At the event, students will learn how to apply for SPROUT and NSF I-Corps grants available through Brandeis Innovation. They will be shown current projects of NSF I-Corps Fellows and have the opportunity to network with potential mentors in the private industry and entrepreneurial sectors. Finally, they will get a review of their CV and be able to speak directly to the Brandeis Innovation Center team about available support and resources for their research.

There will be a series of panels during the day, all sharing their professional and personal experiences, giving advice and guidance. Each panelist has been in the shoes of a recent graduate, looking for their next move after their PhD or postdoc. These panelists have succeeded in crafting unique, rewarding careers for themselves and are here to share their wisdom. There is plenty of time to interact with these panelists one on one, with Q&A sessions after every presentation and intimate lunch sessions with the speakers. Many panelists have openings on their research teams, so attending HackMyPhD is a great way for recent PhD graduates to find opportunities post-graduation.

Students will receive a great deal of valuable professional guidance from attending this event. They will get a professional headshot, a review of their CV, and can also discuss possible startup ideas based on their research.

The keynote speech, delivered by Jonathan Thon, PhD, is guaranteed to be illuminating! His talk will revolve around dispelling common myths that surround research-based business. He asserts that working in industry/startups doesn’t mean that industry dictates research; it is actually scientist-driven, and academic integrity is preserved.

HackMyPhD will be a helpful and engaging event that every student should attend! Sign up today: http://www.hackmyphd.org

Julia Kardon Joins Biochemistry as Assistant Professor

Julia Kardon has joined the Department of Biochemistry as an assistant professor.  Her research addresses the molecular mechanisms that control the activity and quality of mitochondrial proteins to match the dynamic needs of eukaryotic cells. She discovered that a mitochondrial chaperone (ClpX) activates a conserved biosynthetic enzyme through partial unfolding. This discovery poses testable models for how protein unfolding can be controlled and limited and thus how protein unfoldases can direct diverse transformations of their substrates. Her lab will employ diverse biochemical and biophysical approaches to delineate molecular mechanisms of chaperone-mediated control of mitochondrial protein activity, in combination with cell biological, genetic, and proteomic tools to discover new components of mitochondrial protein regulation and quality control.

Julia performed her postdoctoral research with Tania Baker at MIT. She received a Ph.D. in Cell Biology from the University of California, San Francisco with Ron Vale and a B.S. in Molecular Biophysics and Biochemistry from Yale University.

Niels Bradshaw is new Assistant Professor in Biochemistry

Niels Bradshaw, Assistant Professor of BiochemistryNiels Bradshaw has joined the Biochemistry Department as an assistant professor. Protein phosphorylation is a conserved mechanism that controls cell physiology. Niels has uncovered mechanisms that control a widespread family of protein phosphatases and direct them to their targets. Using mechanistic enzymology, structural biology, genetics, and cell biology, his research group will address how phosphatases and other signaling proteins have evolved and diversified to control important processes in all kingdoms of life.

Niels conducted postdoctoral research with Richard Losick at Harvard University. He received his PhD in Biochemistry at the University of California, San Francisco with Peter Walter, and a B.A. in Biology from the University of Chicago.

Paradis and Van Hooser labs collaborate on eLife paper

Figure 3 from research paper

Figure 3. Rem2 is required for late-phase critical period ocular dominance plasticity.

“Rem2 stabilizes intrinsic excitability and spontaneous firing in visual circuits.” Anna R Moore, Sarah E Richards, Katelyn Kenny, Leandro Royer, Urann Chan, Kelly Flavahan, Stephen D Van Hooser, Suzanne Paradis. eLife 2018;7:e33092.

Throughout our waking hours, we experience an ever-changing stream of input from our senses. The brain responds to this varying input by adjusting its own activity levels and even its own structure. It does this by changing the strength of the connections between neurons, or the properties of the neurons themselves. Known as plasticity, this process of continuous change enables the brain to develop, learn and to recover from injury.

The visual systems of mammals are particularly well suited to studying how sensory experience alters the brain. Studies in animals show that lack of sensory input to one or both eyes during a critical period in development causes long-lasting changes in the brain’s visual circuits. Similarly, children with the condition amblyopia or ‘lazy eye’ – in which one eye has impaired vision and the brain ignores input from that eye – can end up with permanent deficits in their vision if the condition is not treated during childhood. Changes in sensory input are thought to trigger plasticity in the brain by altering the activity of specific genes. But exactly how this process works is unclear.

Anna Moore, Sarah Richards et al. now show that a gene called Rem2 has an important role in regulating visual plasticity. In the key experiments, young mice had their vision in one eye blocked for a few days. Analysis of their brains showed that mice that had been genetically modified to lack the Rem2 gene responded differently to this change in their environment (i.e. the loss of input to one eye) than their normal counterparts. Further experiments suggest that Rem2 regulates the excitability of individual neurons: that is, how much the neurons respond to any given input. In the absence of Rem2, neurons in visual areas of the brain become hyperactive. This prevents them from adjusting their activity levels in response to changes in sensory input, which in turn leads to impaired plasticity.

Being able to harness the brain’s visual plasticity mechanisms on demand, for example by regulating Rem2 activity, could benefit individuals with disorders such as amblyopia. Rem2 is also active in many other parts of the brain besides those that support vision. This suggests that manipulating this gene could affect numerous forms of plasticity. However, various barriers must be overcome before we could use this approach to treat brain disorders. These include obtaining a more in depth understanding of the role of the Rem2 gene in the human brain.

Science Posse Scholars Present Posters July 9 at SSC Atrium

Student at Science Posse Session

On July 9th, incoming Science Posse Scholars will be presenting posters on various research topics including pheromones, computational models of galaxies, and software engineering.  The event will take place in the Shapiro Science Center atrium from 1:30 to 3:00 PM. The 10 scholars are interested in pursuing STEM degrees and will all start here at Brandeis in the fall.

Everyone is encouraged to attend.

Melissa Kosinski-Collins Promoted to Professor of Biology

Melissa Kosinski-CollinsMelissa Kosinski-Collins was recently promoted to Professor of Biology. Melissa joined the Biology faculty in 2006 as an Assistant Professor (outside the tenure structure).

Using her passion for teaching, she has updated the undergraduate laboratory curriculum to a system of project-based experiments.  Currently, she is teaching the introductory biology lab course, plant biology, and a graduate level structural biology course.  Melissa is the academic director of the Science Posse and Galaxy Project.

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