JMJ24 antagonizes histone H3K9 demethylase IBM1/JMJ25 function and interacts with RNAi pathways for gene silencing

Publication date: November 2017
Source:Gene Expression Patterns, Volumes 25–26
Author(s): Laure Audonnet, Yuan Shen, Dao-Xiu Zhou
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.



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