Luke Berchowitz
Columbia University, NY·Biochemistry
Amyloids, tightly packed fibrous clumps of protein, are best known as the toxic deposits found in diseases such as Alzheimer's, Parkinson's, and transthyretin cardiac amyloidosis. Yet amyloid-like assemblies can also do useful work in healthy cells, and some cells can build and dismantle them on purpose.
- Fields
Biochemistry
Genetics
Biology
- Topics
amyloid
Rim4
RNA-binding protein
- Grants
- 1 known grant, through Jul 2027
What they work on
- Determine the molecular mechanism by which multi-site phosphorylation rapidly reverses amyloid-like Rim4 into oligomers and monomers at the onset of meiosis II in budding yeast.
- Identify the signals and pathways that trigger assembly of the RNA-binding protein Rim4 into amyloid-like structures, using genetic screens built on selection-based reporters.
- Explain how amyloid-like Rim4 assemblies repress translation of target mRNAs, including retrotransposon mRNAs, using fluorescence reporters in single cells and biochemical approaches.
More about the research
Learning how healthy cells control when these structures form, what they do, and how they are reversed could shed light on why amyloids go wrong in disease.
Why it matters
Few, if any, effective preventive therapies exist for amyloid-related diseases such as Alzheimer's, Parkinson's, and transthyretin cardiac amyloidosis. Understanding how healthy cells naturally build and reverse amyloid-like assemblies could clarify causes of neurodegenerative disease and may point to leads for future therapies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Fei Wang
University of Texas Southwestern Medical Center, TX·Biology
Determine how autophagy, the cell's self-digestion system, promotes gametogenesis in Saccharomyces cerevisiae across meiosis entry, DNA replication, meiosis exit and spore membrane formation, using yeast genetics, biochemistry and imaging.
Gloria Ann Brar
University of California-Berkeley, CA·Genetics
Map how protein complexes are broken down, rebuilt and reorganized as budding yeast form gametes, using proteomics to create an atlas of the parts that are reset during this natural rejuvenation.
Amy MacQueen
Wesleyan University, CT·Genetics
Define how the N terminus of Zip1, a synaptonemal complex building block, works with the Zip3 SUMO ligase to promote crossover recombination in budding yeast, using structure-function genetic analysis.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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