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Biomedical subjects

Junmei Wang

Publications and source records attributed to Junmei Wang.

2 recordsLinked to original sources

Analysis of deep-resequencing data of 984 soybean accessions reveals structural variations underlying agronomic traits.

Genomic structural variants (SVs) are major sources of genetic variation and have profound impacts on phenotypic traits. However, their functional effects remain largely unexplored in soybean. Here, we resequence 940 soybean accessions. Together with 44 publicly available datasets, we identify 602,281 SVs. Using a graph-based genome, we detect an additional 58,760 presence/absence variations (PAVs) that broadly affect gene expression. Population genomic analyses reveal that SVs serve as a core driving force for soybean domestication and improvement. Integrating SVs with QTLs for oil and protein content, and performing GWAS on 27 traits, we identify key functional SVs. These include transposable element insertions altering seed coat color, multiple insertions within a cytochrome P450 gene modifying flower and hypocotyl color, and a GmMATE1 deletion enhancing seed size. Together, our study establishes a comprehensive SV map of soybean, offering a valuable resource for dissecting the genetic basis of complex traits to accelerate molecular breeding.

Glycine max

EZH2 variants derived from cryptic splice sites govern distinct epigenetic patterns during embryonic development.

EZH2 catalyzes H3K27me3 and is essential for embryonic development. Although multiple EZH2 variants have been identified, the functional implications and physiological significance of its heterogeneity remain unclear. Here, we revealed that conserved cryptic splice sites generated two EZH2 variants with (EZH2A) or without (EZH2B) a 27-nt region, coding for a 9-aa segment. Structural modeling showed that splice-in or splice-off of the 9-aa segment caused a topological change in EZH2 structure. The 9-aa surplus in EZH2A strengthened its interaction with other PRC2 components, particularly in PRC2.2 holocomplex. We developed point-mutation mouse lines specifically depleting EZH2A or EZH2B (Ezh2amut or Ezh2bmut). Biallelic deletion of Ezh2a caused developmental defects and embryonic lethality between E12.5 and E15.5, while the Ezh2bmut mice were fertile and developed normally. Combined RNA-seq and CUT&Tag analyses in mouse embryonic fibroblasts revealed that EZH2A and EZH2B bound to different genomic loci and affected H3K27me3 deposition in different subsets of genes related to development or the innate immune system, respectively. EZH2A depletion specifically suppressed the expression of genes involved in the development-related Hippo-Yap1 pathway, which might be attributable to a compensatory process mediated by JARID2. Our findings demonstrate that EZH2 heterogeneity from the 9-aa splicing event plays a crucial role in development.

Animals