Alternative splicing of basic chitinase gene PR3b is regulated in part by the NIC loci in the low-nicotine mutants of Nicotiana tabacum L.cv.Burley 21
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- 英文论文题名：Alternative splicing of basic chitinase gene PR3b is regulated in part by the NIC loci in the low-nicotine mutants of Nicotiana tabacum L.cv.Burley 21
- 论文作者：张鼎宇 ; Yongqiang Ding ; Haoran Ma ; Feng Wang ; Wenjing Wang ; Guoying Yin ; Michael P.Timko ; 张洪波
- 英文论文作者：Dingyu Zhang ; Yongqiang Ding ; Haoran Ma ; Feng Wang ; Wenjing Wang ; Guoying Yin ; Michael P.Timko ; Hongbo Zhang ; College of Agronomy and Biotechnology ; Southwest University ; Tobacco Research Institute ; Chinese Academy of Agricultural Sciences ; Department of Biology ; University of Virginia
- 年：2016
- 作者机构：西南大学;中国农业科学院烟草研究所;Department of Biology,University of Virginia;
- 英文论文关键词：Tobacco ; Low-nicotine mutant ; PR3b ; Alternative splicing ; Jasmonate ; Ethylene
- 会议召开时间：2016-09-25
- 会议录名称：第九届全国核糖核酸学术讨论会论文集
- 语种：英文
- 分类号：Q78
- 学会代码：IGSS
- 会议名称：第九届全国核糖核酸学术讨论会
- 会议地点：中国上海
- 主办单位：中国生物化学与分子生物学会核糖核酸专业委员会
- 学会名称：中国生物化学与分子生物学会
- 页数：1
- 文件大小：175k
- 原文格式：D
- 会议级别：全国
摘要
Two unlinked semi-dominant loci,A(NIC1)and B(NIC2),control nicotine and related alkaloid biosynthesis in Burley tobaccos.Mutations in either or both loci(nic1 and nic2)lead to low nicotine phenotypes with altered environmental stress responses.Here we show that the transcripts derived from the pathogenesis-related(PR)protein gene PR3b are alternatively spliced to a greater extent in nic1 and nic2 mutants and nic1nic2 double mutant of Burley 21.The alternative splicing results in a deletion of 65 nucleotides and introduces a premature stop codon into the coding region of PR3b that leads to a significant reduction of PR3b specific chitinase activity.Further PR3b splicing assays with F2 individuals derived from crosses between nic1 and nic2 mutants and wild type plants supported a genetic linkage to the NIC1 and NIC2 loci,even though NIC1 and NIC2 are unlinked loci.Moreover,the transcriptional analyses showed that the splicing patterns of PR3b in the low-nicotine mutants were differentially regulated by jasmonate(JA)and ethylene(ET).These data suggest that the NIC1 and NIC2 loci display differential roles in regulating the alternative splicing of PR3b in Burley 21.The findings in this study have unraveled valuable information for extending the genetic studies in low-nicotine mutants of Burley 21,and provided clues to unravel the mechanism by which JA and ET signaling pathways post-transcriptionally regulate the activity of PR3b protein.
Two unlinked semi-dominant loci,A(NIC1) and B(NIC2),control nicotine and related alkaloid biosynthesis in Burley tobaccos.Mutations in either or both loci(nic1 and nic2) lead to low nicotine phenotypes with altered environmental stress responses.Here we show that the transcripts derived from the pathogenesis-related(PR) protein gene PR3 b are alternatively spliced to a greater extent in nic1 and nic2 mutants and nic1nic2 double mutant of Burley 21.The alternative splicing results in a deletion of 65 nucleotides and introduces a premature stop codon into the coding region of PR3 b that leads to a significant reduction of PR3 b specific chitinase activity.Further PR3 b splicing assays with F2 individuals derived from crosses between nic1 and nic2 mutants and wild type plants supported a genetic linkage to the NIC1 and NIC2 loci,even though NIC1 and NIC2 are unlinked loci.Moreover,the transcriptional analyses showed that the splicing patterns of PR3 b in the low-nicotine mutants were differentially regulated by jasmonate(JA) and ethylene(ET).These data suggest that the NIC1 and NIC2 loci display differential roles in regulating the alternative splicing of PR3 b in Burley 21.The findings in this study have unraveled valuable information for extending the genetic studies in low-nicotine mutants of Burley 21,and provided clues to unravel the mechanism by which JA and ET signaling pathways post-transcriptionally regulate the activity of PR3 b protein.
Two unlinked semi-dominant loci,A(NIC1) and B(NIC2),control nicotine and related alkaloid biosynthesis in Burley tobaccos.Mutations in either or both loci(nic1 and nic2) lead to low nicotine phenotypes with altered environmental stress responses.Here we show that the transcripts derived from the pathogenesis-related(PR) protein gene PR3 b are alternatively spliced to a greater extent in nic1 and nic2 mutants and nic1nic2 double mutant of Burley 21.The alternative splicing results in a deletion of 65 nucleotides and introduces a premature stop codon into the coding region of PR3 b that leads to a significant reduction of PR3 b specific chitinase activity.Further PR3 b splicing assays with F2 individuals derived from crosses between nic1 and nic2 mutants and wild type plants supported a genetic linkage to the NIC1 and NIC2 loci,even though NIC1 and NIC2 are unlinked loci.Moreover,the transcriptional analyses showed that the splicing patterns of PR3 b in the low-nicotine mutants were differentially regulated by jasmonate(JA) and ethylene(ET).These data suggest that the NIC1 and NIC2 loci display differential roles in regulating the alternative splicing of PR3 b in Burley 21.The findings in this study have unraveled valuable information for extending the genetic studies in low-nicotine mutants of Burley 21,and provided clues to unravel the mechanism by which JA and ET signaling pathways post-transcriptionally regulate the activity of PR3 b protein.
引文