Publications by authors named "Wiam Merini"

Polycomb group (PcG) complexes ensure that every cell in an organism expresses the genes needed at a particular stage, time, or condition. However, it is still not fully understood how PcG complexes PcG-repressive complex 1 (PRC1) and PRC2 are recruited to target genes in plants. Recent findings in Arabidopsis thaliana support the notion that PRC2 recruitment is mediated by different transcription factors (TFs).

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H2A.Z variant has emerged as a critical player in regulating plant responses to environment; however, the mechanism by which H2A.Z mediates this regulation remains unclear.

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Polycomb Group regulation in Arabidopsis (Arabidopsis thaliana) is required to maintain cell differentiation and allow developmental phase transitions. This is achieved by the activity of three PcG repressive complex 2s (PRC2s) and the participation of a yet poorly defined PRC1. Previous results showed that apparent PRC1 components perform discrete roles during plant development, suggesting the existence of PRC1 variants; however, it is not clear in how many processes these components participate.

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Polycomb group (PcG) proteins play important roles in regulating developmental phase transitions in plants; however, little is known about the role of the PcG machinery in regulating the transition from juvenile to adult phase. Here, we show that Arabidopsis (Arabidopsis thaliana) B lymphoma Moloney murine leukemia virus insertion region1 homolog (BMI1) POLYCOMB REPRESSIVE COMPLEX1 (PRC1) components participate in the repression of microRNA156 (miR156). Loss of AtBMI1 function leads to the up-regulation of the primary transcript of MIR156A and MIR156C at the time the levels of miR156 should decline, resulting in an extended juvenile phase and delayed flowering.

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Polycomb group (PcG) proteins constitute a major epigenetic mechanism for gene repression throughout the plant life. For a long time, the PcG mechanism has been proposed to follow a hierarchical recruitment of PcG repressive complexes (PRCs) to target genes in which the binding of PRC2 and the incorporation of H3 lysine 27 trimethyl marks led to recruitment of PRC1, which in turn mediated H2A monoubiquitination. However, recent studies have turned this model upside-down by showing that PRC1 activity can be required for PRC2 recruitment and H3K27me3 marking.

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