Functional integrity of the SEL1L-HRD1 complex is critical for ERAD and organismal viability.

The SEL1L-HRD1 complex represents the most evolutionarily conserved branch of endoplasmic reticulum-associated degradation (ERAD), with SEL1L acting as a key cofactor for the E3 ubiquitin ligase HRD1. While the physiological relevance of this complex has been increasingly recognized, whether SEL1L is strictly required for HRD1 function in mammals has remained unclear. Here, using complementary in vivo and in vitro approaches, we define the architecture and physiological significance of the mammalian SEL1L-HRD1 ERAD complex.

SEL1L-HRD1 ER-Associated Degradation Facilitates Prohormone Convertase 2 Maturation and Glucagon Production in Islet α Cells.

Proteolytic cleavage of proglucagon by prohormone convertase 2 (PC2) is required for islet α cells to generate glucagon. However, the regulatory mechanisms underlying this process remain largely unclear. Here, we report that SEL1L-HRD1 endoplasmic reticulum (ER)-associated degradation (ERAD), a highly conserved protein quality control system responsible for clearing misfolded proteins from the ER, plays a key role in glucagon production by regulating turnover of the nascent proform of the PC2 enzyme (proPC2).

Characterization of the CBM50 Gene Family in and Identification of the Putative Effector Gene ThCBM50_1.

Carbohydrate-binding modules (CBMs) are essential virulence factors in phytopathogens, particularly the extensively studied members from the CBM50 gene family, which are known as lysin motif (LysM) effectors and which play crucial roles in plant-pathogen interactions. However, the function of CBM50 in has yet to be fully studied. In this study, we identified seven CBM50 genes from the genome through complete sequence analysis and functional annotation.

Regulation of leptin signaling and diet-induced obesity by SEL1L-HRD1 ER-associated degradation in POMC expressing neurons.

Endoplasmic reticulum (ER) homeostasis in the hypothalamus has been implicated in the pathogenesis of diet-induced obesity (DIO) and type 2 diabetes; however, the underlying molecular mechanism remain vague and debatable. Here we report that SEL1L-HRD1 protein complex of the highly conserved ER-associated protein degradation (ERAD) machinery in POMC-expressing neurons ameliorates diet-induced obesity and its associated complications, partly by regulating the turnover of the long isoform of Leptin receptors (LepRb). Loss of SEL1L in POMC-expressing neurons attenuates leptin signaling and predisposes mice to HFD-associated pathologies including fatty liver, glucose intolerance, insulin and leptin resistance.

Comparative secretome analysis of different smut fungi and identification of plant cell death-inducing secreted proteins from Tilletia horrida.

Background: Tilletia horrida is a basidiomycete fungus that causes rice kernel smut, one of the most important rice diseases in hybrid rice growing areas worldwide. However, little is known about its mechanisms of pathogenicity. We previously reported the genome of T.

Transcriptome analysis reveals the host selection fitness mechanisms of the Rhizoctonia solani AG1IA pathogen.

Rhizoctonia solani AG1IA is a major generalist pathogen that causes sheath blight. Its genome, which was the first to be sequenced from the Rhizoctonia genus, may serve as a model for studying pathogenic mechanisms. To explore the pathogen-host fitness mechanism of sheath-blight fungus, a comprehensive comparative transcriptome ecotype analysis of R.

Complete genome sequence of Bacillus thuringiensis HS18-1.

Bacillus thuringiensis is a spore-forming bacterium that is a type of insect pathogen used in the field of microbial insect control. B. thuringiensis HS18-1 has effective toxicity for Lepidoptera and Diptera insects.