[No authors listed]
As sessile organisms, plants have evolved multiple mechanisms to respond to environmental changes to improve survival. Arabidopsis plants show accelerated flowering at increased temperatures. Here we show that Jumonji-C domain-containing protein JMJ30 directly binds to the flowering-repressor FLOWERING LOCUS C (FLC) locus and removes the repressive histone modification H3 lysine 27 trimethylation (H3K27me3). At elevated temperatures, the JMJ30 RNA and protein are stabilized, and FLC expression is maintained at high levels to prevent extreme precocious flowering. The double mutant of JMJ30 and its homologue JMJ32, grown at elevated temperatures, exhibits an early-flowering phenotype similar to the flc mutant, which is associated with increased H3K27me3 levels at the FLC locus and decreased FLC expression. Furthermore, ectopic expression of JMJ30 causes an FLC-dependent late-flowering phenotype. Taken together, JMJ30/JMJ32-mediated histone demethylation at the FLC locus constitutes a balancing mechanism in flowering control at warm temperatures to prevent premature early flowering.
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