Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
The replication-dependent histone H3.1 variant, ubiquitous in multicellular eukaryotes, has been proposed to play key roles during chromatin replication due to its unique expression pattern restricted to the S phase of the cell cycle. Here, we describe recent discoveries in plants regarding molecular mechanisms and cellular pathways involving H3.1 that contribute to the maintenance of genomic and epigenomic information. First, we highlight new advances concerning the contribution of the histone chaperone CAF-1 and the TSK-H3.1 DNA repair pathway in preventing genomic instability during replication. We then summarize the evidence connecting H3.1 to specific roles required for the mitotic inheritance of epigenetic states. Finally, we discuss the recent identification of a specific interaction between H3.1 and DNA polymerase epsilon and its functional implications.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11168788 | PMC |
http://dx.doi.org/10.1016/j.pbi.2023.102401 | DOI Listing |
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