Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
98%
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Living organisms are constantly at the risk of DNA damage caused by factors such as DNA replication errors, reactive oxygen species, and UV radiation. In plants, DNA damage activates the NAC-type transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) that governs DNA damage responses such as cell cycle arrest, stem cell death, and early onset of endoreplication. However, molecular mechanisms underlying the early induction of endoreplication onset in response to DNA damage remain elusive. In this study, we show that CELL CYCLE SWITCH 52 A1 (CCS52A1), an activator of the APC/C E3 ligase, plays a major role in the early onset of endoreplication in response to DNA double-strand breaks (DSBs) in Arabidopsis roots. Upon DSBs, SOG1 directly binds to the CCS52A1 locus, thereby inducing its expression. Moreover, early transition to endoreplication in response to DSBs is suppressed in ccs52a1 knockout roots. Our data propose that increased polyploidy may function as a unique adaptative mechanism to genotoxic stress in plants.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238086 | PMC |
http://dx.doi.org/10.1007/s10265-025-01630-y | DOI Listing |