Disease relevance of HSF3

• This analysis demonstrates that (1) raffinose content in leaves increases upon heat stress in wild-type but not in the GolS1 mutant plants; and (2) the level of raffinose is enhanced and stachyose is present at normal temperature in HSF3 TPs [1].

High impact information on HSF3

• Functional consequences of GolS1 expression were investigated by the quantification of raffinose, stachyose, and galactinol contents in wild type, HSF3 TPs, and two different GolS1 knockout mutants (gols1-1 and gols1-2) [1].
• Overexpression of HSF3 or HSF3-GUS, but not of HSF4 or HSF4-GUS, causes HSP synthesis at the non-heat-shock temperature of 25 degrees C in transgenic Arabidopsis [2].
• Electrophoretic mobility shift assays suggest that derepression of the heat shock response is mediated by HSF3/HSF3-GUS functioning as transcription factor [2].
• Complete and selective loss of the promoter binding activities of AtHSF1 or AtHSF3, verified by immunoprecipitation assays, had no obvious effects on the heat shock (HS) response in the individual mutant lines [3].

Biological context of HSF3

• We report the isolation of two HSF genes, HSF3 and HSF4, from an Arabidopsis cDNA library [2].
• Our data indicate that AtHSF1 and AtHSF3 are key regulators of the immediate stress-induced activation of HS gene transcription, and consequently determine the kinetics of the negative feed back loop that is responsible for the transience of HS gene expression in wild type [3].

Analytical, diagnostic and therapeutic context of HSF3

• Derepression of HSF activity upon overexpression suggests the titration of a negative regulator of HSF3 or an intrinsic constitutive activity of HSF3 [2].

References