Some of our recent publications (descriptions are mine, not the authors’)
Lau: Finding new insect viruses by sequencing small RNAs (siRNA and piRNA)
Sengupta Lab: Stress early in life causes epigenetic changes in worms
Drosha and Pasha
February 28, 2009 By
No, this isn’t a Russian short story.
Lead authors postdoc alum Sebastian Kadener and Mol Cell Biol graduate student Joe Rodriguez and their coworkers used tiling arrays to look for targets of the enzyme Drosha in “Genome-wide identification of targets of the drosha–pasha/DGCR8 complex”, a paper recently published in the journal RNA. Drosha is a type III RNAse that is involved in the processing of miRNAs. This paper demonstrates for first time that this enzyme is not only involved in miRNA processing, but can also process mRNAs. Interestingly, the best example of an mRNA processed by Drosha is the mRNA that encodes another miRNA processing enzyme, the protein Pasha. As this is a partner of Drosha (the two proteins work together), the findings suggest that there is a feedback loop that controls the abundance of the miRNA processing machinery and probably the abundance of miRNAs themselves.
Is my DNA fixed yet?
January 29, 2009 By
A broken chromosome (a double-strand DNA break) activates the DNA damage checkpoint to prevent cells from carrying out mitosis until the break has been repaired. Repair of the break involves the modification and the removal of histone protein octamers from DNA around the break and these must be reestablished when repair is complete. In a new paper in PNAS, Brandeis alumnus Jung-Ae Kim (Ph.D., Molecular and Cell Biology, 2008) and Professor James Haber show that when two of the major histone chaperone protein complexes (Asf1 and CAF-1) are deleted in yeast cells, their absence prevents cells from turning off the DNA damage checkpoint and hence cells stay permanently arrested. These results suggest that cells specifically monitor the re-establishment of normal chromatin status after DNA repair.
How actin networks assemble in cells
January 29, 2009 By
A new review article in Current Opinion in Cell Biology by Molecular and Cell Biology grad student Melissa Chesarone and Biology’s Professor Bruce Goode focuses on a group of remarkable protein machines that rapidly assemble actin polymers in cells. These factors are essential for cell division, cell movement, and cell shape determination in virtually all organisms. Their catalytic mechanisms involve intricate fast-moving parts, which enables them to construct entire actin networks in a matter of seconds.
Recent Grant Awards
January 14, 2009 By
Neuroscience Ph.D. candidate Melanie Gainey received an NRSA Fellowship from NINDS. Working in the Turrigiano lab, Melanie plans to study the role of the AMPA receptor subunit GluR2 in synaptic scaling in cultural neurons and in vivo using a conditional GluR2 knockout mouse.
Assistant Professor Suzanne Paradis received a Smith Family New Investigator Award from the Richard & Susan Smith Family Foundation. $300,000 in support over three years will support the lab’s efforts to study synapse development and specifically the role of the Sema4B protein in controlling synapse formation.
Professor Leslie Griffith received $1.1 million over 5 years from NIMH to study why sleep is required for effective memory formation. To understand this linkage at a cellular and molecular level, the Griffith lab is defining the circuits that regulate sleep in Drosophila and how these circuits affect memory formation.
Professor Larry Wangh received $1.38 million over the next year from Smiths Detection to continue research and invention of LATE-PCR et al., platform technologies for highly informative detection and diagnosis of nucleic acids in a single tube. There are ongoing projects looking at applications to cancer, prenatal genetics, and several infectious diseases in people and animals.
Sigma factors
January 8, 2009 By
In a new study appearing in PNAS this week, Brandeis Molecular and Cell Biology graduate student Houra Merrikh and co-workers from the Lovett lab identified the E.coli gene iraD as a regulator of the response to oxidative DNA damage in exponentially growing bacteria. Interestingly, the mechanism seems to involve the alternative RNA polymerase sigma factor RpoS, previously characterized as a regulator of expression during the “stationary phase”. Merrikh et al. argue that this response works in parallel with the previously characterized SOS response in protecting growing bacteria from DNA damage.
