"An epigenetic timer regulates the transition from cell division to cel" by Ruirui Huang

Date of Award

Spring 2024

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Molecular, Cellular, and Developmental Biology

First Advisor

Irish, Vivian

Abstract

Epigenetic changes, such as histone modifications or DNA methylation, can modify gene expression without affecting the genetic code. Such alterations can persist for many cell generations, and often are induced by various environmental inputs in both plants and animals. A number of studies have demonstrated that epigenetic factors regulate plant developmental timing in response to environmental changes. However, we still have an incomplete view of how epigenetic factors can regulate developmental events such as organogenesis, and the transition from cell division to cell expansion, in plants. The small number of cell types and the relatively simple developmental progression required to form the Arabidopsis petal makes it a good model to investigate the molecular mechanisms driving plant organogenesis. It has been found that RABBIT EARS (RBE) temporally regulates petal organogenesis by maintaining cell division at early stages and repressing the activity of key cell division regulators. However, the molecular mechanisms underlying the transcriptional timing of RBE target genes is still unclear. The goal of my thesis project is to identify and investigate the novel players coordinating with RBE to regulate transcription and the epigenetic mechanisms associated with the transcriptional delay induced by RBE. In my thesis project, I investigated how the RBE transcriptional repressor maintains the downregulation of its downstream direct target, TCP5, long after RBE expression dissipates. I showed that RBE recruits the Groucho/Tup1-like corepressor TOPLESS (TPL) and histone deacetylase 19 (HDA19) to repress TCP5 transcription in petal primordia. This process involves multiple layers of changes such as remodeling of chromatin accessibility, alteration of RNA polymerase activity, and histone modifications, resulting in an epigenetic memory that is maintained through multiple cell divisions. This memory functions to maintain cell divisions during the early phase of petal development, and its attenuation in a cell division-dependent fashion later in development enables the transition from cell division to cell expansion. Overall, my thesis project unveils a novel mechanism by which the memory of an epigenetic state, and its cell-cycle regulated decay, acts as a timer to precisely control organogenesis.

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