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BLM's balancing act and the involvement of FANCJ in DNA repair

机译：BLM的平衡法和FANCJ在DNA修复中的参与

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Timely recruitment of DNA damage response proteins to sites of genomic structural lesions is very important for signaling mechanisms to activate appropriate cell cycle checkpoints but also repair the altered DNA sequence to suppress mutagenesis. The eukaryotic cell is characterized by a complex cadre of players and pathways to ensure genomic stability in the face of replication stress or outright genomic insult by endogenous metabolites or environmental agents. Among the key performers are molecular motor DNA unwinding enzymes known as helicases that sense genomic perturbations and separate structured DNA strands so that replacement of a damaged base or sugar-phosphate backbone lesion can occur efficiently. Mutations in the BLM gene encoding the DNA helicase BLM leads to a rare chromosomal instability disorder known as Bloom's syndrome. In a recent paper by the Sengupta lab, BLM's role in the correction of double-strand breaks (DSB), a particularly dangerous form of DNA damage, was investigated. Adding to the complexity, BLM appears to be a key ringmaster of DSB repair as it acts both positively and negatively to regulate correction pathways of high or low fidelity. The FANCJ DNA helicase, mutated in another chromosomal instability disorder known as Fanconi Anemia, is an important player that likely coordinates with BLM in the balancing act. Further studies to dissect the roles of DNA helicases like FANCJ and BLM in DSB repair are warranted.
机译：及时募集DNA损伤响应蛋白对基因组结构病灶的蛋白质对于激活适当的细胞周期检查点而且还修复改变的DNA序列以抑制诱变的方法非常重要。真核细胞的特征在于复杂的球员和途径，以确保面对复制应力或内源代谢物或环境代谢剂的彻底基因组损伤的基因组稳定性。在关键表现者中，是称为螺旋酶的分子马达DNA退滤酶，称为引发基因组扰动和分离结构化DNA链，从而可以有效地发生替代受损碱或糖磷酸盐骨架病变。 BLM基因中编码DNA Helicate BLM的突变导致稀有染色体不稳定障碍，称为绽放综合症。在最近的Sengupta实验室的纸张中，研究了BLM在双链断裂（DSB）的校正中的作用，研究了一种特别危险的DNA损伤形式。添加到复杂性，BLM似乎是DSB维修的关键Ringmaster，因为它具有正面和负面的作用，以调节高保真度或低保真度的校正途径。在另一种称为FANCONI贫血的染色体不稳定障碍中突变的FANCJ DNA Helicase是一个重要的球员，可能在平衡行为中与BLM坐标。有必要进一步研究解剖DNA螺旋酶如FANDJ和BLM在DSB修复中的作用。

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