Significant achievements have been made in breeding programs for the heavy-panicle-type(HPT)rice(Oryza sativa) in Southwest China. The HPT varieties now exhibit excellent lodging resistance,allowing them to overcome t...Significant achievements have been made in breeding programs for the heavy-panicle-type(HPT)rice(Oryza sativa) in Southwest China. The HPT varieties now exhibit excellent lodging resistance,allowing them to overcome the greater pressures caused by heavy panicles. However, the genetic mechanism of this lodging resistance remains elusive. Here, we isolated a major quantitative trait locus, Panicle Neck Diameter 1(PND1), andidentified the causal gene as GRAIN NUMBER 1 A/CYTOKININ OXIDASE 2(Gn1 A/Os CKX2). The null gn1 a allele from rice line R498(gn1 aR498) improved lodging resistance through increasing the culm diameter and promoting crown root development.Loss-of-function of Gn1 a/Os CKX2 led to cytokinin accumulation in the crown root tip and accelerated the development of adventitious roots. Gene pyramiding between the null gn1 aR498 allele with two gain-of-function alleles, STRONG CULM 2(SCM2)and SCM3, further improved lodging resistance.Moreover, Gn1 a/Os CKX2 had minimal influence on overall rice quality. Our research thus highlights the distinct genetic components of lodging resistance of HPT varieties and provides a strategy for tailormade crop improvement of both yield and lodging resistance in rice.展开更多
以常规籼稻品种扬稻6号为材料,在盆栽条件下,于生长锥伸长期外喷6-苄基腺嘌呤(6-BA)后,定期取样,测量穗部细胞分裂素(cytok in ins,CKs)含量,同时采用RT-PCR检测水稻穗分化过程中细胞分裂素氧化酶基因(O sCKX2)的表达模式,考察水稻穗部...以常规籼稻品种扬稻6号为材料,在盆栽条件下,于生长锥伸长期外喷6-苄基腺嘌呤(6-BA)后,定期取样,测量穗部细胞分裂素(cytok in ins,CKs)含量,同时采用RT-PCR检测水稻穗分化过程中细胞分裂素氧化酶基因(O sCKX2)的表达模式,考察水稻穗部性状。结果发现:6-BA处理促进水稻穗长发育并显著提高每穗枝梗和颖花数,分化枝梗数和总颖花数分别为60和255.4,比对照分别提高了10%和30.5%。穗部细胞分裂素含量的增加,刺激了更多颖花分化。6-BA处理的水稻穗部O sCKX2表达时间提前,但表达量下降。认为:水稻穗分化始期喷施6-BA可降低穗部O sCKX2的表达强度,提高穗部细胞分裂素含量,对枝梗和颖花分化产生促进作用,为形成大穗提供了先决条件。展开更多
Grain number is a flexible trait and contributes significantly to grain yield.In rice,the zinc finger transcription factor DROUGHT AND SALT TOLERANCE(DST)controls grain number by directly regulating cytokinin oxidase!...Grain number is a flexible trait and contributes significantly to grain yield.In rice,the zinc finger transcription factor DROUGHT AND SALT TOLERANCE(DST)controls grain number by directly regulating cytokinin oxidase!dehydrogenase 2(OsCKX2)expression.Although specific upstream regulators of the DST-OsCKX2 module have been identified,the mechanism employed by DST to regulate the expression of OsCKX2 remains unclear.Here,we demonstrate that DST-interacting protein 1(DIP1),known as Mediator subunit OsMED25,acts as an interacting coactivator of DST.Phenotypic analyses revealed that OsMED25-RNAi and the osmed25 mutant plants exhibited enlarged panicles,with enhanced branching and spikelet number,similar to the dst mutant.Genetic analysis indicated that OsMED25 acts in the same pathway as the DST-OsCKX2 module to regulate spikelet number per panicle.Further biochemical analysis showed that OsMED25 physically interacts with DST at the promoter region of OsCKX2,and then recruits RNA polymerase II(Pol II)to activate OsCKX2 transcription.Thus,OsMED25 was involved in the communication between DST and Pol II general transcriptional machinery to regulate spikelet number.In general,our findings reveal a novel function of OsMED25 in DST-OsCKX2 modulated transcriptional regulation,thus enhancing our un derstanding of the regulatory mechanism underlying DST-OsCKX2-mediated spikelet number.展开更多
基金supported by the National Natural Science Foundation of China(92535301)Sichuan Science and Technology Program(2021YJ0501)。
文摘Significant achievements have been made in breeding programs for the heavy-panicle-type(HPT)rice(Oryza sativa) in Southwest China. The HPT varieties now exhibit excellent lodging resistance,allowing them to overcome the greater pressures caused by heavy panicles. However, the genetic mechanism of this lodging resistance remains elusive. Here, we isolated a major quantitative trait locus, Panicle Neck Diameter 1(PND1), andidentified the causal gene as GRAIN NUMBER 1 A/CYTOKININ OXIDASE 2(Gn1 A/Os CKX2). The null gn1 a allele from rice line R498(gn1 aR498) improved lodging resistance through increasing the culm diameter and promoting crown root development.Loss-of-function of Gn1 a/Os CKX2 led to cytokinin accumulation in the crown root tip and accelerated the development of adventitious roots. Gene pyramiding between the null gn1 aR498 allele with two gain-of-function alleles, STRONG CULM 2(SCM2)and SCM3, further improved lodging resistance.Moreover, Gn1 a/Os CKX2 had minimal influence on overall rice quality. Our research thus highlights the distinct genetic components of lodging resistance of HPT varieties and provides a strategy for tailormade crop improvement of both yield and lodging resistance in rice.
基金supported by the National Key Research and Development Program of China (Grant No. 2019YFD1000300)Agricultural Seed Project of Shandong Province (Grant Nos 2020LZGC005, 2021LZGC0017)+1 种基金the Tai-Shan Scholar Program from Shandong Province (Grant No. tsxk20150901)the K. C. Wong Education Foundation.
文摘Grain number is a flexible trait and contributes significantly to grain yield.In rice,the zinc finger transcription factor DROUGHT AND SALT TOLERANCE(DST)controls grain number by directly regulating cytokinin oxidase!dehydrogenase 2(OsCKX2)expression.Although specific upstream regulators of the DST-OsCKX2 module have been identified,the mechanism employed by DST to regulate the expression of OsCKX2 remains unclear.Here,we demonstrate that DST-interacting protein 1(DIP1),known as Mediator subunit OsMED25,acts as an interacting coactivator of DST.Phenotypic analyses revealed that OsMED25-RNAi and the osmed25 mutant plants exhibited enlarged panicles,with enhanced branching and spikelet number,similar to the dst mutant.Genetic analysis indicated that OsMED25 acts in the same pathway as the DST-OsCKX2 module to regulate spikelet number per panicle.Further biochemical analysis showed that OsMED25 physically interacts with DST at the promoter region of OsCKX2,and then recruits RNA polymerase II(Pol II)to activate OsCKX2 transcription.Thus,OsMED25 was involved in the communication between DST and Pol II general transcriptional machinery to regulate spikelet number.In general,our findings reveal a novel function of OsMED25 in DST-OsCKX2 modulated transcriptional regulation,thus enhancing our un derstanding of the regulatory mechanism underlying DST-OsCKX2-mediated spikelet number.
