Abstract

Stress-induced regulation of flowering time insures evolutionary fitness. Stress-induced late flowering is thought to result from a plant evoking tolerance mechanism to wait out the stress before initiating reproduction. Stress-induced early flowering, on the other hand, is thought to be a stress-escape response. By shortening their life cycle to produce seeds before severe stress leads to death, this insures survival of the species at the cost of lower seed yield. Previously, we reported that overexpression of OXS3 (OXIDATIVE STRESS 3) could enhance tolerance to cadmium and oxidizing agents in Arabidopsis whereas an oxs3 null mutant was slightly more sensitive to these chemicals. In this study, we found that the absence of OXS3 also causes early flowering under a mild drought stress treatment. This contrasts with the behavior of wild type Ws4 and Col ecotypes that responded to the same condition by delaying flowering time. We tested the hypothesis that OXS3 might ordinarily exert a negative regulatory role on flowering during drought stress, which in its absence, would lead to stress-induced early flowering. In a search of whether OXS3 could interfere with regulators that activate flowering, we found that OXS3 could bind SOC1 in vitro and in vivo. Overexpression of OXS3 in a transient expression assay was found to repress the AP1 promoter, and the full repression effect required SOC1. It is possible that the OXS3/SOC1 interaction serves to prevent precocious flower development and prevent low seed set from a premature stress-induced flowering response.

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