Back to Search Start Over

Unequally redundant RCD1 and SRO1 mediate stress and developmental responses and interact with transcription factors.

Authors :
Jaspers P
Blomster T
Brosché M
Salojärvi J
Ahlfors R
Vainonen JP
Reddy RA
Immink R
Angenent G
Turck F
Overmyer K
Kangasjärvi J
Source :
The Plant journal : for cell and molecular biology [Plant J] 2009 Oct; Vol. 60 (2), pp. 268-79. Date of Electronic Publication: 2009 Jun 22.
Publication Year :
2009

Abstract

RADICAL-INDUCED CELL DEATH1 (RCD1) is an important regulator of stress and hormonal and developmental responses in Arabidopsis thaliana. Together with its closest homolog, SIMILAR TO RCD-ONE1 (SRO1), it is the only Arabidopsis protein containing the WWE domain, which is known to mediate protein-protein interactions in other organisms. Additionally, these two proteins contain the core catalytic region of poly-ADP-ribose transferases and a conserved C-terminal domain. Tissue and subcellular localization data indicate that RCD1 and SRO1 have partially overlapping functions in plant development. In contrast mutant data indicate that rcd1 has defects in plant development, whereas sro1 displays normal development. However, the rcd1 sro1 double mutant has severe growth defects, indicating that RCD1 and SRO1 exemplify an important genetic principle - unequal genetic redundancy. A large pair-wise interaction test against the REGIA transcription factor collection revealed that RCD1 interacts with a large number of transcription factors belonging to several protein families, such as AP2/ERF, NAC and basic helix-loop-helix (bHLH), and that SRO1 interacts with a smaller subset of these. Full genome array analysis indicated that in many cases targets of these transcription factors have altered expression in the rcd1 but not the sro1 mutant. Taken together RCD1 and SRO1 are required for proper plant development.

Details

Language :
English
ISSN :
1365-313X
Volume :
60
Issue :
2
Database :
MEDLINE
Journal :
The Plant journal : for cell and molecular biology
Publication Type :
Academic Journal
Accession number :
19548978
Full Text :
https://doi.org/10.1111/j.1365-313X.2009.03951.x