Sridevi Sureshkumar, Monash University
Sridevi Sureshkumar
Keynote speaker
Monash University

Sridevi uses Arabidopsis thaliana as a system to study epigenetic gene silencing caused by expanded DNA repeats. Her research group focuses on epigenetic regulation and an environmental response in plants, and she is interested in understanding the mechanisms of alternative splicing in the context of the evolution of phenotypes.

Sureshkumar holds a Ph.D. in Plant Molecular Biology from the Max-Planck Institute for Developmental Biology in Tuebingen, Germany. Sureshkumar's research interests focus on understanding the regulation of gene expression in plants. She later joined Monash University with an ARC-ADP fellowship to investigate the function of alternative splicing in the thermal response of plants and trinucleotide repeat expansion-mediated gene regulation. Her latest work centers on the mechanisms of trinucleotide repeat expansion in plants, for which she received an ARC-Future fellowship. Over the years, Sureshkumar developed Arabidopsis as a model to study the mechanisms underlying repeat expansions causal for phenotypic variability."

Research interests: Arabidopsis, gene regulation, epigenetics, trinucleotide repeat expansions, and environmental responses.
Poster Number / Talk Time

Session 7

Abstract:

The molecular mechanisms of trinucleotide expansions- a role for SUMO proteases.

Arabidopsis wild strain Bur-0 exhibits a temperature-sensitive phenotype known as irregularly impaired leaves (iil), which is caused by the expansion of GAA/TTC intronic trinucleotide repeat at the IIL1 locus. This results in transcriptional downregulation and similar to the intronic repeat expansion seen in the human genetic disorder Friedreich ataxia. By conducting a genetic suppressor screening, we identified FUG1, an uncharacterized SUMO protease that plays a key role in suppressing IIL1 expression and cause epigenetic silencing. Using Bio-chemical assays we discovered that FUG1 protease physically interacts with histone reader AL3, which in turn interacts with the PRC1 complex component LHP1 to cause a chromatin state switch from the active chromatin into inactive chromatin and promote gene silencing at the IIL1 locus. Our findings reveal novel genes and mechanisms of epigenetic silencing caused by expanded repeats which has implications not only for plants but also for human genetic disorders.