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Wang, G.-S.

Publications and source records attributed to Wang, G.-S..

2 recordsLinked to original sources

Proposal of two new genera and seventy-seven new species of ascomycetous yeasts isolated from China

Ascomycetous yeasts belong to Saccharomycotina and Taphrinomycotina, with about 1,200 described species distributed worldwide. More than 300 ascomycetous yeast species have been reported from China, which indicates that China possesses a hotspot with high yeast diversity. However, our knowledge of yeast diversity and distribution remains limited, and this area needs to be explored in depth. Here we describe 77 new ascomycetous yeast species with 195 isolates obtained over the past two decades during the continuous yeast diversity surveys in China, based on the phylogenetic analyses of the sequences of D1/D2 domains of the large subunit (LSU) and the internal transcribed spacer region including the 5.8S rDNA (ITS) of the nuclear ribosomal DNA (rDNA). The average nucleotide identity (ANI) analysis was used to delimitate closely related species with low sequence heterogeneity in the ITS and D1/D2 regions. Seventy-five of these new species belong to 35 genera in the Saccharaomycotina, while the other two are distributed in Taphrina of the Taphrinomycotina. In addition, we propose two new genera, namely Gaboromyces gen. nov. and Yurkovozyma gen. nov.

microbiology↗

Neurodegeneration induces a developmental RNA processing program by calpain-mediated MBNL2 degradation

The Muscleblind-like (MBNL) protein family plays an important role in regulating developmental RNA processing transition. Loss of MBNL2 function has been implicated in the neurodegeneration of myotonic dystrophy type 1 (DM1). However, the causal mechanism of neurodegeneration-induced MBNL2 loss of function remains elusive. Here, we show that neurodegenerative conditions including NMDAR-mediated excitotoxicity and dysregulated calcium homeostasis triggered nuclear translocation of calpain-2 resulting in MBNL2 degradation and reversion of MBNL2-regulated RNA processing to developmental patterns. The developmental stage featured nucleus-enriched distribution of calpain-2 and low expression of MBNL2. Increased MBNL2 expression during development is required for promoting developmental RNA processing transition and neuronal maturation. Knockdown of calpain-2 expression inhibited neurodegeneration-induced MBNL2 reduction and dysregulated RNA processing. Neurodegenerative disease mouse models including DM1 and Alzheimers disease showed nuclear translocation of calpain-2 associated with MBNL2 degradation and reversion of MBNL2-regulated RNA processing to the developmental pattern. Our results identify a novel regulatory mechanism for MBNL2 downregulation and suggest that reduced MBNL2 expression accompanied by the re-induction of a developmental RNA processing program may be a common feature of neurodegeneration.

neuroscience↗