{"title":"H3R2me2a去甲基化酶JMJ10通过与转录因子BZR1.3相互作用调控番茄果实大小。","authors":"Jing Zeng,Zhiwei Li,Xiaochun Ding,Hanzhi Liang,Keqiang Wu,Yueming Jiang,Xuewu Duan,Guoxiang Jiang","doi":"10.1093/plcell/koaf251","DOIUrl":null,"url":null,"abstract":"Fruit weight and size are fundamental traits in tomato breeding and critical determinants of yield. Although several histone-modifying enzymes have been implicated in tomato fruit ripening, the role of histone arginine methylation in fruit development remains unknown. Here, we identify the histone H3R2me2a demethylase Jumonji C-domain-containing proteins 10 (JMJ10) as a key regulator of fruit size in tomato (Solanum lycopersicum). Loss of JMJ10 function reduces fruit size, whereas JMJ10 overexpression enhances fruit growth, primarily by promoting pericarp cell expansion. JMJ10 specifically demethylates H3R2me2a at key fruit size-associated genes, including FW11.3, CDF4, EXP2, EXP5, XTH8, and PRE2, thereby promoting their transcription. Furthermore, we show that JMJ10 physically interacts with the transcription factor Brassinazole-Resistant 1.3 (BZR1.3), which recruits JMJ10 to its target genes. The jmj10 bzr1.3 double mutants exhibit a more severe reduction in fruit size compared to either single mutant, confirming a synergistic interaction between JMJ10 and BZR1.3. ChIP-qPCR analysis showed that JMJ10 occupancy at its target loci is significantly reduced in the bzr1.3 mutant, suggesting that JMJ10 binding is BZR1.3-dependent. Additionally, BZR1.3 recruits JMJ10 to enhance the expression of these genes by facilitating H3R2me2a removal. Collectively, our findings reveal a mechanism by which BZR1.3 recruits JMJ10, a H3R2me2a demethylase, to coordinate the epigenetic regulation of fruit size in tomato.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":"8 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The H3R2me2a demethylase JMJ10 regulates tomato fruit size through its interaction with the transcription factor BZR1.3.\",\"authors\":\"Jing Zeng,Zhiwei Li,Xiaochun Ding,Hanzhi Liang,Keqiang Wu,Yueming Jiang,Xuewu Duan,Guoxiang Jiang\",\"doi\":\"10.1093/plcell/koaf251\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Fruit weight and size are fundamental traits in tomato breeding and critical determinants of yield. Although several histone-modifying enzymes have been implicated in tomato fruit ripening, the role of histone arginine methylation in fruit development remains unknown. Here, we identify the histone H3R2me2a demethylase Jumonji C-domain-containing proteins 10 (JMJ10) as a key regulator of fruit size in tomato (Solanum lycopersicum). Loss of JMJ10 function reduces fruit size, whereas JMJ10 overexpression enhances fruit growth, primarily by promoting pericarp cell expansion. JMJ10 specifically demethylates H3R2me2a at key fruit size-associated genes, including FW11.3, CDF4, EXP2, EXP5, XTH8, and PRE2, thereby promoting their transcription. Furthermore, we show that JMJ10 physically interacts with the transcription factor Brassinazole-Resistant 1.3 (BZR1.3), which recruits JMJ10 to its target genes. The jmj10 bzr1.3 double mutants exhibit a more severe reduction in fruit size compared to either single mutant, confirming a synergistic interaction between JMJ10 and BZR1.3. ChIP-qPCR analysis showed that JMJ10 occupancy at its target loci is significantly reduced in the bzr1.3 mutant, suggesting that JMJ10 binding is BZR1.3-dependent. Additionally, BZR1.3 recruits JMJ10 to enhance the expression of these genes by facilitating H3R2me2a removal. Collectively, our findings reveal a mechanism by which BZR1.3 recruits JMJ10, a H3R2me2a demethylase, to coordinate the epigenetic regulation of fruit size in tomato.\",\"PeriodicalId\":501012,\"journal\":{\"name\":\"The Plant Cell\",\"volume\":\"8 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-10-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Plant Cell\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/plcell/koaf251\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Plant Cell","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/plcell/koaf251","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
果实重量和大小是番茄育种的基本性状,也是决定产量的关键因素。虽然有几种组蛋白修饰酶与番茄果实成熟有关,但组蛋白精氨酸甲基化在果实发育中的作用尚不清楚。本研究发现组蛋白H3R2me2a去甲基化酶Jumonji c -domain containing proteins 10 (JMJ10)是番茄果实大小的关键调控因子。JMJ10功能缺失会降低果实大小,而JMJ10过表达则主要通过促进果皮细胞扩张来促进果实生长。JMJ10特异性地使H3R2me2a在果实大小相关的关键基因上去甲基化,包括FW11.3、CDF4、EXP2、EXP5、XTH8和PRE2,从而促进它们的转录。此外,我们发现JMJ10与转录因子Brassinazole-Resistant 1.3 (BZR1.3)发生物理相互作用,从而将JMJ10招募到其靶基因。与单突变体相比,jmj10 bzr1.3双突变体表现出更严重的果实大小减少,证实了jmj10和bzr1.3之间的协同相互作用。ChIP-qPCR分析显示,在bzr1.3突变体中,JMJ10在其靶位点的占用率显著降低,表明JMJ10的结合依赖于bzr1.3。此外,BZR1.3招募JMJ10通过促进H3R2me2a的去除来增强这些基因的表达。总之,我们的研究结果揭示了BZR1.3招募H3R2me2a去甲基化酶JMJ10来协调番茄果实大小表观遗传调控的机制。
The H3R2me2a demethylase JMJ10 regulates tomato fruit size through its interaction with the transcription factor BZR1.3.
Fruit weight and size are fundamental traits in tomato breeding and critical determinants of yield. Although several histone-modifying enzymes have been implicated in tomato fruit ripening, the role of histone arginine methylation in fruit development remains unknown. Here, we identify the histone H3R2me2a demethylase Jumonji C-domain-containing proteins 10 (JMJ10) as a key regulator of fruit size in tomato (Solanum lycopersicum). Loss of JMJ10 function reduces fruit size, whereas JMJ10 overexpression enhances fruit growth, primarily by promoting pericarp cell expansion. JMJ10 specifically demethylates H3R2me2a at key fruit size-associated genes, including FW11.3, CDF4, EXP2, EXP5, XTH8, and PRE2, thereby promoting their transcription. Furthermore, we show that JMJ10 physically interacts with the transcription factor Brassinazole-Resistant 1.3 (BZR1.3), which recruits JMJ10 to its target genes. The jmj10 bzr1.3 double mutants exhibit a more severe reduction in fruit size compared to either single mutant, confirming a synergistic interaction between JMJ10 and BZR1.3. ChIP-qPCR analysis showed that JMJ10 occupancy at its target loci is significantly reduced in the bzr1.3 mutant, suggesting that JMJ10 binding is BZR1.3-dependent. Additionally, BZR1.3 recruits JMJ10 to enhance the expression of these genes by facilitating H3R2me2a removal. Collectively, our findings reveal a mechanism by which BZR1.3 recruits JMJ10, a H3R2me2a demethylase, to coordinate the epigenetic regulation of fruit size in tomato.