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Title: G2 Checkpoint Responses in Arabidopsis

Technical Report ·
DOI:https://doi.org/10.2172/1116357· OSTI ID:1116357
 [1]
  1. Univ. of California, Davis, CA (United States)

This project focused on the mechanism and biological significance of the G2 arrest response to replication stress in plants. We employed both forward and reverse genetic approaches to identify genes required for this response. A total of 3 different postdocs, 5 undergraduates, and 2 graduate students participated in the project. We identified several genes required for damage response in plants, including homologs of genes previously identified in animals (ATM and ATR), novel, a plant-specific genes (SOG1) and a gene known in animals but previously thought to be missing from the Arabidopsis genome (ATRIP). We characterized the transcriptome of gamma-irradiated plants, and found that plants, unlike animals, express a robust transcriptional response to damage, involving genes that regulate the cell cycle and DNA metabolism. This response requires both ATM and the transcription factor SOG1. We found that both ATM and ATR play a role in meiosis in plants. We also found that plants have a cell-type-specific programmed cell death response to ionizing radiation and UV light, and that this response requires ATR, ATM, and SOG1. These results were published in a series of 5 papers.

Research Organization:
Univ. of California, Davis, CA (United States)
Sponsoring Organization:
USDOE
DOE Contract Number:
FG02-05ER15668
OSTI ID:
1116357
Report Number(s):
DOE-DAVIS-15668-2
Country of Publication:
United States
Language:
English

References (4)

A shared DNA-damage-response pathway for induction of stem-cell death by UVB and by gamma irradiation journal September 2010
Both ATM and ATR promote the efficient and accurate processing of programmed meiotic double-strand breaks journal August 2008
Suppressor of gamma response 1 (SOG1) encodes a putative transcription factor governing multiple responses to DNA damage journal June 2009
ATR and ATM play both distinct and additive roles in response to ionizing radiation journal December 2006

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