Transposable elements (TEs), also known as jumping genes, comprise a major portion of eukaryotic genomes, although their functional contribution is still one of biology's big mysteries. Due to the potentially mutagenic nature of their transposition activity, it has been assumed that TEs are heavily suppressed, if not completely silenced, predominantly through epigenetic mechanisms, i.e., non-inheritable chemical modifications introduced into chromosomes. The researchers' analyses suggest, however, that TEs are rapidly and transiently derepressed in response to pathogen infection. Based on these findings, it is hypothesized that TEs play important roles in transcriptional reprogramming/activation in response to biotic stress and that their activity leads to phenotypic plasticity and stress adaptation. For the host plant, the proposed ability of TEs to transduce environmental challenges into epigenetic modifications that lead to stable genetic changes should confer significant evolutionary advantages. Therefore, elucidating the molecular mechanisms through which stress adaptation is mediated by epigenetic changes and clarifying their relationship to TE activation following biotic stress will be tremendously valuable for developing new traits in the plant breeding industry. The proposed research also will allow undergraduate students, as well as high school students and their teachers, to investigate solutions to a real-world problem via experimentation using high-throughput assays that will provide a robust dataset after a limited training period. The results of these analyses will be presented at local, state and national science fairs.

The researchers' analysis of genome-wide chromatin accessibility suggests that the promoters and/or 5' proximal regions of many defense genes contain TEs that display heightened and dynamic chromatin accessibility in Arabidopsis after pathogen infection. These TE-associated chromatin regions exhibit infection-induced dynamic interactions with MORC1, a protein implicated in both RNA-dependent DNA methylation (RdDM) and immunity in plants. Given that i) TEs are suppressed mostly by RdDM, ii) pathogen infection induces a burst of TE expression, and iii) both TE transcription and mobility are modulated by the RdDM pathway, epigenetic factors involved in RdDM will be investigated to test the role(s) of RdDM and TEs in the induction of defense genes following pathogen infection. To this end, specific TEs and RdDM components will be silenced or knocked-out to monitor DNA methylation, chromatin accessibility and transcription levels for both targeted TEs and their proximal defense genes following infection. TEs' role in stress adaptation will also be examined by inducing biotic stress-induced TE transposition and determining if novel TE insertions confer stress-induced transcription of their proximal genes in subsequent generations. Altogether, this project seeks to significantly advance our understanding of the relationship between TEs and both immunity and stress adaptation.

Agency
National Science Foundation (NSF)
Institute
Division of Integrative Organismal Systems (IOS)
Application #
1553613
Program Officer
Michael Mishkind
Project Start
Project End
Budget Start
2016-03-15
Budget End
2022-02-28
Support Year
Fiscal Year
2015
Total Cost
$787,913
Indirect Cost
Name
Texas State University - San Marcos
Department
Type
DUNS #
City
San Marcos
State
TX
Country
United States
Zip Code
78666