2016
DOI: 10.1371/journal.pgen.1006283
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Correction: Mek1 Down Regulates Rad51 Activity during Yeast Meiosis by Phosphorylation of Hed1

Abstract: In the Data Availability statement, the link for accessing the processed recombination analysis files in Dryad is incorrect. The correct link is http://dx.doi.org/10.5061/dryad.g6s2k.

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Cited by 6 publications
(3 citation statements)
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“…We also monitored the activity of the downstream Mek1 effector kinase using three different readouts: Mek1 autophosphorylation (Ontoso et al 2013), Hed1 phosphorylation at T40 (Callender et al 2016), and histone H3 phosphorylation at T11 (Cavero et al 2016). As shown in Figure 4D, the dynamics of Mek1 activation paralleled that of Hop1-T318 phosphorylation (that is, Mec1 activity) and, again, was similar in both zip1 and zip1 htz1, except for a slight persistence of phospho-H3-T11 in zip1 htz1 at the latest time point.…”
Section: Dynamics Of Upstream Checkpoint Activationdeactivation Is Nomentioning
confidence: 99%
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“…We also monitored the activity of the downstream Mek1 effector kinase using three different readouts: Mek1 autophosphorylation (Ontoso et al 2013), Hed1 phosphorylation at T40 (Callender et al 2016), and histone H3 phosphorylation at T11 (Cavero et al 2016). As shown in Figure 4D, the dynamics of Mek1 activation paralleled that of Hop1-T318 phosphorylation (that is, Mec1 activity) and, again, was similar in both zip1 and zip1 htz1, except for a slight persistence of phospho-H3-T11 in zip1 htz1 at the latest time point.…”
Section: Dynamics Of Upstream Checkpoint Activationdeactivation Is Nomentioning
confidence: 99%
“…Previous studies suggest that the eventual checkpoint deactivation and recovery of meiotic progression in zip1 is consequence of the disappearance of the initial defects (likely unrepaired DSBs), presumably by using the sister chromatid instead of the homolog as template for DNA repair. This is based on the observation that deletion of RAD51, which fundamentally compromises sister chromatid recombination (Liu et al 2014;Callender et al 2016), leads to a permanent arrest in zip1 (Herruzo et al 2016) (Figure S7A). In this work we report that, like zip1 rad51, the zip1 htz1 double mutant also shows a tight meiotic block; however, the analysis of various checkpoint markers reveals that the cause of the arrest is different in zip1 rad51 and zip1 htz1.…”
Section: H2az Is Required For Proper Meiotic Developmentmentioning
confidence: 99%
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