RESUMO
Dimethylation of histone H3 lysine 9 (H3K9me2) is a heterochromatic mark linked to DNA methylation and gene repression. Removal of H3K9me2 from gene bodies by the jmjC histone demethylase IBM1/JMJ25 inhibits DNA methylation and derepresses gene expression. In this work, we analyzed the function of a closely related homolog of IBM1/JMJ25, namely JMJ24. We show that jmj24 mutations produced a number of subtle developmental defects, while affecting only a relatively small number of genes at the vegetative stage. Interestingly, jmj24 mutation could complement plant growth defects and expression changes caused by the ibm1 mutation. In addition, we show that JMJ24 may synergistically interact with the RNAi pathways involving siRNAs. The present data suggest that JMJ24 may have a function to counteract IBM1/JMJ25 in gene expression and may cooperate with RNAi pathways for gene silencing.
Assuntos
Proteínas de Arabidopsis/genética , Arabidopsis/crescimento & desenvolvimento , Histona Desmetilases com o Domínio Jumonji/genética , Arabidopsis/genética , Epigênese Genética , Perfilação da Expressão Gênica , Regulação da Expressão Gênica no Desenvolvimento , Regulação da Expressão Gênica de Plantas , Inativação Gênica , Histonas/metabolismo , Mutação , Interferência de RNA , Transdução de SinaisRESUMO
Histone H3 lysine 4 trimethylation (H3K4me3) has been shown to be involved in stress-responsive gene expression and gene priming in plants. However, the role of H3K4me3 resetting in the processes is not clear. In this work we studied the expression and function of Arabidopsis H3K4 demethylase gene JMJ15. We show that the expression of JMJ15 was relatively low and was limited to a number of tissues during vegetative growth but was higher in young floral organs. Over-expression of the gene in gain-of-function mutants reduced the plant height with accumulation of lignin in stems, while the loss-of-function mutation did not produce any visible phenotype. The gain-of-function mutants showed enhanced salt tolerance, whereas the loss-of-function mutant was more sensitive to salt compared to the wild type. Transcriptomic analysis revealed that over-expression of JMJ15 down-regulated many genes which are preferentially marked by H3K4me3 and H3K4me2. Many of the down-regulated genes encode transcription regulators involved in stress responses. The data suggest that increased JMJ15 levels may regulate the gene expression program that enhances stress tolerance.
