{"title":"SOG1 和 BRCA1 相互依赖地调控 RAD54 的表达,以修复拟南芥中盐分诱导的 DNA 双链断裂。","authors":"Kalyan Mahapatra, Sujit Roy","doi":"10.1093/pcp/pcae008","DOIUrl":null,"url":null,"abstract":"<p><p>As sessile organisms, land plants experience various forms of environmental stresses throughout their life span. Therefore, plants have developed extensive and complicated defense mechanisms, including a robust DNA damage response (DDR) and DNA repair systems for maintaining genome integrity. In Arabidopsis, the NAC [NO APICAL MERISTEM (NAM), ARABIDOPSIS TRANSCRIPTION ACTIVATION FACTOR (ATAF), CUP-SHAPED COTYLEDON (CUC)] domain family transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) plays an important role in regulating DDR. Here, we show that SOG1 plays a key role in regulating the repair of salinity-induced DNA double-strand breaks (DSBs) via the homologous recombination (HR) pathway in Arabidopsis. The sog1-1 mutant seedlings display a considerably slower rate of repair of salinity-induced DSBs. Accumulation of SOG1 protein increases in wild-type Arabidopsis under salinity stress, and it enhances the expression of HR pathway-related genes, including RAD51, RAD54 and BReast CAncer gene 1 (BRCA1), respectively, as found in SOG1 overexpression lines. SOG1 binds specifically to the AtRAD54 promoter at the 5'-(N)4GTCAA(N)3C-3' consensus sequence and positively regulates its expression under salinity stress. The phenotypic responses of sog1-1/atrad54 double mutants suggest that SOG1 functions upstream of RAD54, and both these genes are essential in regulating DDR under salinity stress. Furthermore, SOG1 interacts directly with BRCA1, an important component of the HR-mediated DSB repair pathway in plants, where BRCA1 appears to facilitate the binding of SOG1 to the RAD54 promoter. At the genetic level, SOG1 and BRCA1 function interdependently in modulating RAD54 expression under salinity-induced DNA damage. Together, our results suggest that SOG1 regulates the repair of salinity-induced DSBs via the HR-mediated pathway through genetic interactions with RAD54 and BRCA1 in Arabidopsis.</p>","PeriodicalId":20575,"journal":{"name":"Plant and Cell Physiology","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SOG1 and BRCA1 Interdependently Regulate RAD54 Expression for Repairing Salinity-Induced DNA Double-Strand Breaks in Arabidopsis.\",\"authors\":\"Kalyan Mahapatra, Sujit Roy\",\"doi\":\"10.1093/pcp/pcae008\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>As sessile organisms, land plants experience various forms of environmental stresses throughout their life span. Therefore, plants have developed extensive and complicated defense mechanisms, including a robust DNA damage response (DDR) and DNA repair systems for maintaining genome integrity. In Arabidopsis, the NAC [NO APICAL MERISTEM (NAM), ARABIDOPSIS TRANSCRIPTION ACTIVATION FACTOR (ATAF), CUP-SHAPED COTYLEDON (CUC)] domain family transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) plays an important role in regulating DDR. Here, we show that SOG1 plays a key role in regulating the repair of salinity-induced DNA double-strand breaks (DSBs) via the homologous recombination (HR) pathway in Arabidopsis. The sog1-1 mutant seedlings display a considerably slower rate of repair of salinity-induced DSBs. Accumulation of SOG1 protein increases in wild-type Arabidopsis under salinity stress, and it enhances the expression of HR pathway-related genes, including RAD51, RAD54 and BReast CAncer gene 1 (BRCA1), respectively, as found in SOG1 overexpression lines. SOG1 binds specifically to the AtRAD54 promoter at the 5'-(N)4GTCAA(N)3C-3' consensus sequence and positively regulates its expression under salinity stress. The phenotypic responses of sog1-1/atrad54 double mutants suggest that SOG1 functions upstream of RAD54, and both these genes are essential in regulating DDR under salinity stress. Furthermore, SOG1 interacts directly with BRCA1, an important component of the HR-mediated DSB repair pathway in plants, where BRCA1 appears to facilitate the binding of SOG1 to the RAD54 promoter. At the genetic level, SOG1 and BRCA1 function interdependently in modulating RAD54 expression under salinity-induced DNA damage. 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引用次数: 0
摘要
作为无柄生物,陆生植物在其整个生命周期中都会经受各种形式的环境压力。因此,植物发展出了广泛而复杂的防御机制,包括强大的 DNA 损伤应答(DDR)和 DNA 修复系统,以保持基因组的完整性。在拟南芥中,NAC结构域家族转录因子SUPPRESSOR OF GAMMA RESPONSE1(SOG1)在调节DDR中发挥着重要作用。在这里,我们发现 SOG1 在拟南芥中通过同源重组(HR)途径调节盐度诱导的 DNA 双链断裂(DSB)修复中发挥着关键作用。sog1-1突变体幼苗对盐度诱导的DSB的修复速度明显较慢。在盐分胁迫下,野生型拟南芥中 SOG1 蛋白的积累会增加,它能增强 HR 途径相关基因的表达,包括 RAD51、RAD54 和 BRCA1,这一点在 SOG1 过表达株中也有发现。SOG1 与 AtRAD54 启动子的 5'-(N)4GTCAA(N)3C-3' 共识序列特异性结合,并在盐度胁迫下正向调控其表达。sog1-1/atrad54双突变体的表型反应表明,SOG1在RAD54的上游起作用,而这两个基因在盐分胁迫下调控DDR都是必不可少的。此外,SOG1 与 BRCA1 直接相互作用,BRCA1 是植物 HR 介导的 DSB 修复途径的重要组成部分,BRCA1 似乎促进了 SOG1 与 RAD54 启动子的结合。在基因水平上,SOG1和BRCA1在盐度诱导的DNA损伤下调节RAD54表达的功能是相互依存的。总之,我们的研究结果表明,在拟南芥中,SOG1通过与RAD54和BRCA1的基因相互作用,通过HR介导的途径调节盐度诱导的DSB的修复。
SOG1 and BRCA1 Interdependently Regulate RAD54 Expression for Repairing Salinity-Induced DNA Double-Strand Breaks in Arabidopsis.
As sessile organisms, land plants experience various forms of environmental stresses throughout their life span. Therefore, plants have developed extensive and complicated defense mechanisms, including a robust DNA damage response (DDR) and DNA repair systems for maintaining genome integrity. In Arabidopsis, the NAC [NO APICAL MERISTEM (NAM), ARABIDOPSIS TRANSCRIPTION ACTIVATION FACTOR (ATAF), CUP-SHAPED COTYLEDON (CUC)] domain family transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) plays an important role in regulating DDR. Here, we show that SOG1 plays a key role in regulating the repair of salinity-induced DNA double-strand breaks (DSBs) via the homologous recombination (HR) pathway in Arabidopsis. The sog1-1 mutant seedlings display a considerably slower rate of repair of salinity-induced DSBs. Accumulation of SOG1 protein increases in wild-type Arabidopsis under salinity stress, and it enhances the expression of HR pathway-related genes, including RAD51, RAD54 and BReast CAncer gene 1 (BRCA1), respectively, as found in SOG1 overexpression lines. SOG1 binds specifically to the AtRAD54 promoter at the 5'-(N)4GTCAA(N)3C-3' consensus sequence and positively regulates its expression under salinity stress. The phenotypic responses of sog1-1/atrad54 double mutants suggest that SOG1 functions upstream of RAD54, and both these genes are essential in regulating DDR under salinity stress. Furthermore, SOG1 interacts directly with BRCA1, an important component of the HR-mediated DSB repair pathway in plants, where BRCA1 appears to facilitate the binding of SOG1 to the RAD54 promoter. At the genetic level, SOG1 and BRCA1 function interdependently in modulating RAD54 expression under salinity-induced DNA damage. Together, our results suggest that SOG1 regulates the repair of salinity-induced DSBs via the HR-mediated pathway through genetic interactions with RAD54 and BRCA1 in Arabidopsis.
期刊介绍:
Plant & Cell Physiology (PCP) was established in 1959 and is the official journal of the Japanese Society of Plant Physiologists (JSPP). The title reflects the journal''s original interest and scope to encompass research not just at the whole-organism level but also at the cellular and subcellular levels.
Amongst the broad range of topics covered by this international journal, readers will find the very best original research on plant physiology, biochemistry, cell biology, molecular genetics, epigenetics, biotechnology, bioinformatics and –omics; as well as how plants respond to and interact with their environment (abiotic and biotic factors), and the biology of photosynthetic microorganisms.