کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2057955 1076127 2009 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Overexpression of IAA1 with domain II mutation impairs cell elongation and cell division in inflorescences and leaves of Arabidopsis
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم زراعت و اصلاح نباتات
پیش نمایش صفحه اول مقاله
Overexpression of IAA1 with domain II mutation impairs cell elongation and cell division in inflorescences and leaves of Arabidopsis
چکیده انگلیسی

SummaryThe auxin/indoleacetic acid (Aux/IAA) proteins are negative regulators of the auxin response factors (ARFs) that regulate expression of auxin-responsive genes. The Aux/IAA proteins have four conserved domains. Domain II is responsible for the rapid degradation of these proteins. Degradation of the Aux/IAA proteins, mediated by a SCFTIR1 E3 ubiquitin protein ligase complex, is critical for auxin-regulated gene expression. Using a steroid-hormone-inducible system, we had previously shown that a protein-stability-enhancing mutation in domain II of IAA1 (iaa1) impaired diverse auxin responses. Inhibition of hypocotyl elongation, leaf expansion, and stem elongation by overexpression of iaa1 suggested that cell enlargement and/or cell division might be affected. We here examined the effects of the domain II mutation on cellular anatomy using light microscopy. Our results show that overexpression of iaa1 in Arabidopsis significantly reduced cell length and cell number and affected cell shape in inflorescences and leaves in a dexamethasone (DEX)-dependent manner. These results suggest that IAA1 might be involved in cell elongation as well as in cell division in the aerial parts of Arabidopsis plants. In addition, the formation of both phloem and xylem in leaves and stems was also impaired in a DEX-dependent manner, indicating a potential involvement of IAA1 in vascular development.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Plant Physiology - Volume 166, Issue 5, 15 March 2009, Pages 548–553
نویسندگان
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