例如:"lncRNA", "apoptosis", "WRKY"

DNA-binding and repressor function are prerequisites for the turnover of the tomato heat stress transcription factor HsfB1.

Plant J. 2017 Jan;89(1):31-44. doi:10.1111/tpj.13317. Epub 2016 Nov 14
Sascha Röth 1 , Oliver Mirus 1 , Daniela Bublak 1 , Klaus-Dieter Scharf 1 , Enrico Schleiff 2
Sascha Röth 1 , Oliver Mirus 1 , Daniela Bublak 1 , Klaus-Dieter Scharf 1 , Enrico Schleiff 2

[No authors listed]

Author information
  • 1 Molecular Cell Biology of Plants, Goethe University Frankfurt/Main, Max-von-Laue Str. 9, Frankfurt/Main, Germany.
  • 2 Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt/Main, Max-von-Laue Str. 9, Frankfurt/Main, Germany.

摘要


HsfB1 is a central regulator of heat stress (HS) response and functions dually as a transcriptional co-activator of HsfA1a and a general repressor in tomato. HsfB1 is efficiently synthesized during the onset of HS and rapidly removed in the course of attenuation during the recovery phase. Initial results point to a complex regime modulating HsfB1 abundance involving the molecular chaperone Hsp90. However, the molecular determinants affecting HsfB1 stability needed to be established. We provide experimental evidence that DNA-bound HsfB1 is efficiently targeted for degradation when active as a transcriptional repressor. Manipulation of the DNA-binding affinity by mutating the HsfB1 DNA-binding domain directly influences the stability of the transcription factor. During HS, HsfB1 is stabilized, probably due to co-activator complex formation with HsfA1a. The process of HsfB1 degradation involves nuclear localized Hsp90. The molecular determinants of HsfB1 turnover identified in here are so far seemingly unique. A mutational switch of the R/KLFGV repressor motif's arginine and lysine implies that the abundance of other R/KLFGV type Hsfs, if not other transcription factors as well, might be modulated by a comparable mechanism. Thus, we propose a versatile mechanism for strict abundance control of the stress-induced transcription factor HsfB1 for the recovery phase, and this mechanism constitutes a form of transcription factor removal from promoters by degradation inside the nucleus.

KEYWORDS: Arabidopsis thaliana , Solanum lycopersicum , Hsp90, K/RLFGV transcription factor family, abiotic stress response, chaperone function, protein degradation, protein half-life