TinII intron, an enhancer to affect the function of the cytoplasmic male sterility related gene T in Brassica juncea

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• 作者：ZhuPing Jin (1) (2)
  LingLing Wu (1)
  JiaShu Cao (3)
  ZhuJun Chen (3)
  YanXi Pei (1)
  
• 关键词：cytoplasmic male sterility (CMS) ; alternative splicing ; enhancer ; intron
• 刊名：Science China Life Sciences
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：56
• 期：12
• 页码：1107-1112
• 全文大小：
• 作者单位：ZhuPing Jin (1) (2)
  LingLing Wu (1)
  JiaShu Cao (3)
  ZhuJun Chen (3)
  YanXi Pei (1)
  
  1. School of Life Science, Shanxi University, Taiyuan, 030006, China
  2. School of Chemical Engineering and Environment, North University of China, Taiyuan, 030051, China
  3. Institute of Vegetable Science, Zhejiang University, Hangzhou, 310058, China
  
• ISSN：1869-1889

文摘

The T gene, which was cloned from the mitochondria of tumorous stem mustard (Brassica juncea var. tumida), is a cytoplasmic male sterility (CMS)-related gene that can produce two transcripts, T1170 and T1243. The latter is transcribed with the uncleaved intron TinII. In our previous study, transgenic Arabidopsis thaliana plants over-expressing the T1243 transcript (OE-T1243) showed a severe male-sterile phenotype, whereas OE-T1170 plants did not. However, the functional mechanism of the T gene in B. Juncea remained unknown. In this study, microscopic analyses of paraffin sections of anthers confirmed that OE-T1243 plants did not produce normal pollen, whereas OE-T1170 plants did. We analyzed the transcription of 15 anther development-related genes and found that transcript levels of nozzle/sporocyteless and barely any meristem 1 and 2 were markedly lower in OE-T1243 plants than those in wild type, while the transcript levels of these genes in OE-T1170 plants were unchanged. To investigate the potential roles of TinII, we inserted the TinII sequence upstream of a minimal region (60) of the cauliflower mosaic virus 35S promoter fused to the 5end of the glucuronidase (GUS) reporter gene. Analysis of the transgenic plants suggested that TinII acted as an enhancer to significantly increase GUS expression. The potential action mechanism is that the TinII intron acts as an enhancer to affect the function of the CMS-related gene T.