Member Profile

Scott Michaels

Plant Species Used: 
PhD-granting university/college
Associate Professor
Indiana University
Bloomington, IN
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In our laboratory, we use two different models to study the links between histone modifications, chromatin structure, and gene expression. The first model is the constitutive heterochromatin present in Arabidopsis nuclei, which contain repetitive sequences, transposons, and rDNA genes. Histones in chromocenters are marked by modifications that are known to repress gene expression, such as histone H3 monomethylation at lysine 27 (H3K27me1). Our laboratory has identified ATXR5 and ATXR6 as the enzymes that are responsible for H3K27me1 at chromocenters and the loss of these enzymes leads to loss of gene silencing, decondensation of heterochromatin, and fascinatingly, over-replication of discrete regions of the genome. Ongoing work in our lab is elucidating the mechanisms by which the activity of ATXR5 and ATXR6 is targeted to heterochromatin, how H3K27 methylation leads to gene silencing, and the role of chromatin modification in the regulation of DNA replication.

The second model that we use is an epigenetic switch that is triggered by signals from the environment. To ensure that flowering occurs at a favorable time of year, many plants growing in temperate climates have adopted a biennial growth habit. These plants contain a block to flowering that is eliminated by the prolonged cold temperatures of winter; thus flowering is prevented prior to winter and promoted in the favorable conditions of spring. In biennial-like, winter-annual accessions of Arabidopsis, this block to flowering is created by the floral repressor FLOWERING LOCUS C (FLC). Prior to winter, FLC is highly expressed and prevents flowering. Cold treatment, in turn, causes a permanent epigenetic shut off of FLC expression that is mediated by repressive histone modifications at the FLC locus. Our laboratory is actively involved in determining that molecular mechanisms that control this epigenetic switch.


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