MicroRNAs Profiling Reveals a Potential Link between the SDG8 Methyltransferase and Brassinosteroid-Regulated Gene Expression in Arabidopsis

Abstract

Dong and Li, J Data Mining Genomics Proteomics 2013, 4:5http://dx.doi.org/10.4172/2153-0602.1000e110J Data Mining Genomics Proteomics Volume 4 • Issue 5 • 1000e110ISSN: 2153-0602 JDMGP, an open access journalMicroRNAs are a class of short non-coding RNAs (17-27 nucleotides) found in animals and plants. MicroRNAs play important roles in post-transcriptional regulation of gene expression by complementing the target mRNAs and causing translational repression or target mRNA degradation [1]. Studies have shown that thousands of human protein-coding genes are regulated by microRNAs [2], impacting many important biological processes, from development to physiology to stress response. In plants, microRNAs have been implicated in multiple essential biological processes, such as leaf morphogenesis and polarity, flower development, hormone signaling and metabolism, and stress responses [3]. MicroRNA genes are transcribed by RNA polymerases II, generating precursors that undergo a series of cleavage events to form mature microRNA [4]. MicroRNA biogenesis and its expression regulation are highly complicated [5]. Although the biological importance of microRNAs is well demonstrated in a wide range of cellular processes, how microRNA expression and abundance are regulated is not fully understood.Histone modifications play critical roles in regulation of gene expression in eukaryotes [6]. Acetylation of histones H3 and H4 is commonly associated with gene activation, whereas histone deacetylation generally leads to gene silencing. Trimethylation of histone H3 on lysine 4 (H3K4me3) is frequently associated with active transcription, while trimethylation of histone H3 on lysine 27 (H3K27me3) is often associated with gene repression. Trimethylation of histone H3 on lysine 36 (H3K36me3) is usually enriched in coding regions of actively transcribed genes [6], but H3K36me3 also correlates with gene silencing in facultative and constitutive heterochromatin[7].Recent studies in mammalian cells indicate that histone acetylation and methylation affect microRNA expression. Scott et al. [8] first showed that histone deacetylase inhibition results in alteration of microRNA levels in a breast cancer cell line. Following this study, several reports have shown that histone deacetylase inhibition alters microRNA expression in human carcinomas [9-11]. Overexpression of histone deacetylases in chronic lymphocytic leukemia results in silencing of miR-15a, miR-16, and miR-29b, while histone deacetylase inhibition can partially restore the expression of miR-15a, miR-16, and miR-29b[12]. These results collectively show that histone acetylation and deacetylation play important roles in regulation of microRNA expression in human cells. Stable RNAi-mediated suppression of the H3K4me3 demethylaseJARID1B in breast tumor cells caused increased expression of several members of the let-7 family of microRNAs, suggesting that H3K4me3 is required for up-regulation of the expression of these microRNAs [13]. Parallel sequencing analyses show that H3K27me3 is associated with repressed microRNA genes in mouse lymphocytes[14]. Taken together, these studies indicate that histone methylation can modulate microRNA expression.The SET domain group 8 (SDG8) protein is the primary methyltransferase for global histone H3K36 trimethylation in Arabidopsis [15,16]. SDG8 is involved in a number of developmental processes such shoot branching, ovule and anther development, and flowering time [16-18]. To explore the potential role of histone H3K36 trimethylation in the regulation of microRNA expression, we compared the miRNA expression profile of the knockout mutant of the SDG8 methyltransferase (sdg8) with the wild-type (WT) using microRNA microarray technology. MicroRNA microarray analysis was carried out by LC sciences (Houston, Texas, USA) on μParafloTM microfluidics chips containing 154 microRNA probes to