The <i>lba1</i> mutation of UPF1 RNA helicase involved in nonsense‐mediated mRNA decay causes pleiotropic phenotypic changes and altered sugar signalling in Arabidopsis

• Masato Yoine

• Masa‐aki Ohto

• Kiyoshi Onai

• Satoru Mita

• Kenzo Nakamura

抄録

The low‐beta‐amylase1 ( lba1 ) mutant of Arabidopsis thaliana has reduced sugar‐induced expression of At β ‐Amy and shows pleiotropic phenotypes such as early flowering; short day‐sensitive growth; and seed germination that is hypersensitive to glucose and abscisic acid and resistant to mannose. lba1 was a missense mutation of UPF1 RNA helicase involved in nonsense‐mediated mRNA decay (NMD), which eliminates mRNAs with premature termination codons (PTCs), and replaces highly conserved Gly 851 of UPF1 with Glu. Expression of the wild‐type UPF1 in lba1 rescued not only the reduced sugar‐inducible gene expression, but also early flowering and altered seed‐germination phenotypes. Sugar‐inducible mRNAs were over‐represented among transcripts decreased in sucrose‐treated lba1 compared with Col plants, suggesting that UPF1 is involved in the expression of a subset of sugar‐inducible genes. On the other hand, transcripts increased in lba1 , which are likely to contain direct targets of NMD, included mRNAs for many transcription factors and metabolic enzymes that play diverse functions. Among these, the level of an alternatively spliced transcript of AtTFIIIA containing PTC was 17‐fold higher in lba1 compared with Col plants, and it was reduced to the level in Col by expressing the wild‐type UPF1. The lba1 mutant provides a good tool for studying NMD in plants.

収録刊行物

• The Plant Journal

  The Plant Journal 47 (1), 49-62, 2006-06

  Wiley

キーワード

• Cell Biology
• Plant Science
• Genetics

詳細情報

• CRID: 1361137045074882176
• NII論文ID: 30014610387
• DOI: 10.1111/j.1365-313x.2006.02771.x
• ISSN: 1365313X
• ISSN: 09607412
• Web Site: https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-313X.2006.02771.x
• Web Site: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-313X.2006.02771.x
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