Fig. 7: CHH hypermethylation mediates LEC2-induced somatic embryogenesis through the SUVH-SDJ-AHL complex. | Nature Communications

Fig. 7: CHH hypermethylation mediates LEC2-induced somatic embryogenesis through the SUVH-SDJ-AHL complex.

From: LEC2 induces somatic cell reprogramming through epigenetic activation of plant cell totipotency regulators

Fig. 7

Overexpression of LEC2 triggers the upregulation of genes associated with the DRM2-DDR complex, wherein the DDR complex comprises DRD1, DMS3, and RDM1. This activation occurs within the RdDM pathway, leading to maintaining CHH hypermethylation at the promoters of totipotency-regulating genes during somatic embryogenesis. In addition, LEC2 can stimulate the expression of genes that encode the DNA methylation reader complex SUVH-SDJ. This complex recruits AHL chromatin modification proteins, which play a crucial role in directly or indirectly interacting with histone acetyltransferases (HATs)53. This interaction promotes histone acetylation, thereby increasing chromatin accessibility at the promoters of totipotency-regulating genes. Furthermore, the SUVH-SDJ-AHL complex interacts with LEC2, reinforcing LEC2-mediated activation of totipotency-regulating genes and somatic embryogenesis.

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