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Indiana University Bloomington

Department of Biology

Graduate Studies

Genetics, Cellular & Molecular Sciences Training Grant

Trainee Profile

Quincy Williams

Photo of Briana Whitaker
Research Image(s)

promotion of flowering comparison

Promotion of flowering by the autonomous pathway. The autonomous pathway represses the expression of FLC, a floral repressor, allowing for the expression of floral promoters. Note that in late-flowering autonomous-pathway mutants, the plant continues to grow vegetatively, producing a larger number of leaves.

Graduate Student
Contact Information
By telephone: 812-856-0355 (lab)
MY 359
Michaels Lab
Department of Biology:
Genome, Cell & Developmental Biology
B.A. Biology, 2013, Transylvania University
NIH Training Grant in Genetics, Cellular, and Molecular Sciences (2014-2016)
Research Description

Studying the molecular basis of flowering time in plants is important for a variety of reasons, the most broadly of which being that in through understanding how different genes are environmentally regulated, new agricultural and genetic techniques can be engineered to ultimately increase crop yield, or to combat the deleterious effects of climate change.  Flowering time is affected by a variety of pathways, two of which include photoperiod and vernalization.  The major pathway I will be studying is the vernalization pathway, which works in that when exposed to long periods of cold (vernalization), there is a genetic silencing of Flowering Locus C (FLC) which in turn allows for flowering to commence in the spring.

There has been previous work done to show that FLC mRNA transcript pausing and decapping/degradation by exonucleases are essential for FLC regulation.  Furthermore, the Michaels lab has done work to show that some of these decapping proteins act in a complex and may be responsible in part for an early flowering phenotype.  For my research, I will use a variety of genetic and biochemical techniques to identify how FLC is differentially regulated in mutants of these aforementioned proteins then use that information to build a model in which FLC transcriptional pausing/degradation is controlled via these proteins.


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