<b>Event image data for 'Separable roles of the DNA damage response kinase Mec1</b>^{<strong>ATR</strong>}<b> </b><b>and its activator Rad24</b>^{<strong>RAD17</strong>}<b> </b><b>during meiotic recombination'</b>

Data for paper published in PLoS Genetics (date pending)<b>S4 Data</b> Event images for all strains and meioses studied.<b>Abstract</b>During meiosis, programmed DNA double-strand breaks (DSBs) are formed by the topoisomerase-like enzyme, Spo11, activating the DNA damage response (DDR) kinase Mec1ATR via the checkpoint clamp loader, Rad24RAD17. At single loci, loss of Mec1 and Rad24 activity alters DSB formation and recombination outcome, but their genome-wide roles have not been examined in detail. Here, we utilise two strategies—deletion of the mismatch repair protein, Msh2, and control of meiotic prophase length via regulation of the Ndt80 transcription factor—to help characterise the roles Mec1 and Rad24 play in meiotic recombination by enabling genome-wide mapping of meiotic progeny. In line with previous studies, we observe severely impacted spore viability and a reduction in the frequency of recombination upon deletion of RAD24—driven by a shortened prophase. By contrast, loss of Mec1 function increases recombination frequency, consistent with its role in DSB trans-interference, and has less effect on spore viability. Despite these differences, complex multi-chromatid events initiated by closely spaced DSBs—rare in wild-type cells—occur more frequently in the absence of either Rad24 or Mec1, suggesting a loss of spatial regulation at the level of DSB formation in both. Mec1 and Rad24 also have important roles in the spatial regulation of crossovers (COs). Upon loss of either Mec1 or Rad24, CO distributions become more random—suggesting reductions in the global manifestation of interference. Such effects are similar to, but less extreme than, the phenotype of ‘ZMM’ mutants such as zip3∆, and may be driven by reductions in the proportion of interfering COs. Collectively, in addition to shared roles in CO regulation, our results highlight separable roles for Rad24 as a pro-CO factor, and for Mec1 as a regulator of recombination frequency, the loss of which helps to suppress any broader defects in CO regulation caused by abrogation of the DDR.

本数据集对应发表于《PLoS Genetics》（发表日期待定）的论文的<b>S4数据集</b>，包含所有研究菌株及减数分裂过程的事件图像。<b>摘要</b>减数分裂过程中，类拓扑异构酶Spo11会诱导形成程序性DNA双链断裂（double-strand breaks, DSBs），并通过检查点夹加载因子Rad24RAD17激活DNA损伤应答（DNA damage response, DDR）激酶Mec1ATR。在单基因座层面，Mec1与Rad24的功能缺失会改变DSB形成与重组结局，但二者在全基因组层面的作用尚未得到详细研究。本研究利用两种策略——缺失错配修复蛋白Msh2，以及通过调控Ndt80转录因子控制减数分裂前期时长——实现减数分裂子代的全基因组定位，以此解析Mec1与Rad24在减数分裂重组中的作用。与既往研究一致，我们观察到RAD24缺失会导致孢子存活率严重受损，且重组频率降低，这一现象由减数分裂前期缩短所驱动。与之相反，Mec1功能缺失会提升重组频率，这与其在DSB反式干扰中的作用相符，且对孢子存活率的影响较弱。尽管存在上述差异，在野生型细胞中罕见的、由紧密间隔的DSB引发的复杂多染色质事件，在Rad24或Mec1缺失的细胞中发生频率更高，这表明二者在DSB形成层面均丧失了空间调控能力。Mec1与Rad24在交换（crossovers, COs）的空间调控中同样发挥重要作用。当Mec1或Rad24功能缺失时，CO的分布变得更为随机，这提示全局干扰水平有所下降。此类效应与zip3∆等"ZMM"突变体的表型相似，但程度更轻，其成因可能是具有干扰效应的CO比例降低。综上，除了在CO调控中存在共同作用外，我们的研究结果还揭示了Rad24作为促交换因子、Mec1作为重组频率调控因子的可分离功能；Mec1的缺失有助于抑制因DDR功能丧失所引发的CO调控的广泛缺陷。

搜集汇总

背景与挑战

背景概述

该数据集提供了一篇关于减数分裂重组中DNA损伤响应激酶Mec1ATR及其激活因子Rad24RAD17可分离作用的研究论文的事件图像数据，包含所有菌株和减数分裂过程的图像，用于支持基因组范围内的重组分析。数据涉及减数分裂中DNA双链断裂的形成、重组频率调控以及交叉事件的空间分布，旨在揭示Mec1和Rad24在减数分裂中的不同角色，如Rad24作为促交叉因子而Mec1调控重组频率。数据集发布于2024年，采用CC BY 4.0许可证开放共享。