Nucleocytoplasmic OXIDATIVE STRESS 2 can relocate FLOWERING LOCUS T.

Survival of a species depends on reproductive fitness and a plant's floral transition is controlled by developmental and environmental signals. In Arabidopsis, the floral integrators SOC1 (SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1) and FT (FLOWERING LOCUS T) sense various pathway signals to activate floral meristem identity genes. At high stress intensity, greater nuclear accumulation of the zinc-finger transcription factor OXS2 (OXIDATIVE STRESS 2) activates an early-flowering stress-escape response. Curiously, accumulation of OXS2 in the cytoplasm can delay flowering, prompting the hypothesis that in absence of stress, OXS2 helps to maintain vegetative growth. While the mechanism of stress-escape was identified as the OXS2-mediated transcription of SOC1, how cytoplasmic OXS2 delays flowering was unknown. Here, we report that OXS2 can interact indirectly with florigen FT and transcription factor FD (FLOWERING LOCUS D), the two proteins known to induce floral transition. By using 14-3-3Ω as a bridge linker, OXS2 can alter the subcellular distribution of FT. This lead to a speculation on how cytoplasmic OXS2 is able to prevent early flowering, by keeping FT from the nucleus.

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