TRICHOMELESS1 regulates trichome patterning by suppressingGLABRA1inArabidopsis
Author(s) -
Shucai Wang,
Su-Hwan Kwak,
Qingning Zeng,
Brian E. Ellis,
XiaoYa Chen,
John Schiefelbein,
JinGui Chen
Publication year - 2007
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.009597
Subject(s) - biology , arabidopsis , transcription factor , ectopic expression , microbiology and biotechnology , myb , trichome , chromatin immunoprecipitation , mutant , epidermis (zoology) , phenotype , chromatin , genetics , gene expression , gene , botany , promoter , anatomy
The patterning of epidermal cell types in Arabidopsis is a simple and useful model for studying the molecular basis of cell specification in plants. The distribution of different cell types in the Arabidopsisepidermis is regulated by a lateral inhibition mechanism that relies on interactions between transcription factors. However, it is unclear how temporal- or organ-specific differences in epidermal patterning are achieved. Here we identify TRICHOMELESS1 (TCL1) as a new and major single-repeat MYB-type transcription factor that negatively regulates trichome formation in the inflorescence epidermis. A dominant mutant with elevated expression of TCL1 has a glabrous (trichomeless) phenotype, whereas a loss-of-function mutation in TCL1 uniquely confers ectopic trichome formation on inflorescence stem and pedicels. Genetic analyses demonstrate that TCL1 and CAPRICE work synergistically to regulate trichome patterning on these organs. Interestingly, overexpression of TCL1 specifically suppresses the expression of GLABRA1 (GL1), a crucial component in the trichome initiation complex, whereas loss-of-function of TCL1enhances GL1 expression. Chromatin immunoprecipitation results show that TCL1 can be recruited to the cis-acting regulatory elements of GL1. These results provide the first molecular and genetic evidence that an R3 MYB may negatively regulate trichome cell specification in a novel manner by directly suppressing the transcription of GL1.
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