Loading…
Over-expression of the Arabidopsis AtMYB41 gene alters cell expansion and leaf surface permeability
The Arabidopsis AtMYB41 gene encodes an R2R3-MYB transcription factor whose expression is not detectable under normal growth conditions in any organ or at any developmental stage analysed. It is expressed at high levels in response to drought, ABA and salt treatments, suggesting a possible role in s...
Saved in:
Published in: | The Plant journal : for cell and molecular biology 2008-01, Vol.53 (1), p.53-64 |
---|---|
Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The Arabidopsis AtMYB41 gene encodes an R2R3-MYB transcription factor whose expression is not detectable under normal growth conditions in any organ or at any developmental stage analysed. It is expressed at high levels in response to drought, ABA and salt treatments, suggesting a possible role in stress responses. Transgenic lines over-expressing this transcription factor showed a pleiotropic phenotype similar to that exhibited by some mutants that affect cuticle biosynthesis. This includes a dwarf appearance, dependent on smaller cells with abnormal morphology, enhanced sensitivity to desiccation, and enhanced permeability of leaf surfaces, suggesting discontinuity in the cuticle. The expression of genes involved in lipid metabolism and transport, in cell-wall modifications and cell expansion, genes coding for membrane-associated proteins and genes specifically involved in cuticle metabolism was differentially modulated between wild-type and transgenic plants, suggesting a direct or indirect role of AtMYB41 in the regulation of their transcription. Taken together, our results suggest that AtMYB41 is part of a complex network of transcription factors controlling cell expansion and cuticle deposition in response to abiotic stress. |
---|---|
ISSN: | 0960-7412 1365-313X |
DOI: | 10.1111/j.1365-313x.2007.03310.x |