当前位置:主页 > 科技论文 > 基因论文 >

海岛棉转录因子基因GbMYB60的克

发布时间:2018-05-07 16:38

  本文选题:棉花 + MYB转录因子 ; 参考:《作物学报》2016年09期


【摘要】:MYB转录因子是在真核生物细胞内广泛存在的一类转录因子蛋白,在植物的生长发育、代谢调节、抗病抗逆、以及激素介导的信号路径等方面都发挥着重要的作用。本研究从海岛棉品种海7124中克隆得到一个MYB转录因子基因,根据序列同源性和进化分析,将其命名为GbMYB60。该基因序列长990 bp,编码一个36.9 k D的R2R3类MYB转录因子蛋白。GbMYB60蛋白被特异地定位于植物细胞核。GbMYB60基因的表达水平较低,在真叶中优势表达,根系中表达量最低。该基因受甘露醇、Na Cl、低温、高温等非生物逆境,以及脱落酸、乙烯利、茉莉酸甲酯和水杨酸等植物激素的诱导上调表达。利用病毒诱导的基因沉默技术在海岛棉中干涉GbMYB60发现,降低GbMYB60基因的表达水平,使棉花幼苗对高盐胁迫的耐受性降低;但GbMYB60干涉的植株在甘露醇溶液的处理下与对照植株并无显著的抗性差异。
[Abstract]:MYB transcription factors are a class of transcription factor proteins widely existing in eukaryotic cells, which play an important role in plant growth and development, metabolic regulation, disease resistance and stress resistance, as well as hormone mediated signal pathway. A MYB transcription factor gene was cloned from sea island cotton variety Hai 7124 and named GbMYB60 according to sequence homology and evolution analysis. The length of the gene was 990 BP, encoding a 36.9 KD R2R3 like transcription factor protein. GbMYB60 protein was specifically located in the plant nucleus. The expression level of GbMYB60 gene was lower than that in the true leaves, and the lowest in the root system. The gene was up-regulated by abiotic stresses such as mannitol, low temperature, high temperature, and plant hormones such as abscisic acid, ethephon, methyl jasmonate and salicylic acid. The technique of virus-induced gene silencing was used to interfere with GbMYB60 in island cotton. It was found that the expression level of GbMYB60 gene was decreased and the tolerance of cotton seedlings to high salt stress was decreased. However, there was no significant difference in resistance between the plants treated with mannitol and the control plants treated with GbMYB60 interference.
【作者单位】: 河南大学生命科学学院/棉花生物学国家重点实验室/植物逆境生物学重点实验室;
【基金】:国家重点基础研究发展计划项目(2012CB1143001) 棉花生物学国家重点实验室开放课题(CB2015A31) 河南省教育厅项目(15A180028,15A180029)资助~~
【分类号】:S562


本文编号:1857662

资料下载
论文发表

本文链接:https://www.wllwen.com/kejilunwen/jiyingongcheng/1857662.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户31e09***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com