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S. cerevisiae Mub1, a substrate adaptor of E3 ubiquitin ligase, modulates sensitivity to cell wall stressors through multiple transcription factors

ABSTRACT: S. cerevisiae Mub1, a substrate adaptor of E3 ubiquitin ligase, modulates sensitivity to cell wall stressors through multiple transcription factors

PROVIDER: PRJNA1111539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29024525_1.fastq.gz	Fastqsanger.gz
	SRR29024525_2.fastq.gz	Fastqsanger.gz
	SRR29024526_1.fastq.gz	Fastqsanger.gz
	SRR29024526_2.fastq.gz	Fastqsanger.gz
	SRR29024527_1.fastq.gz	Fastqsanger.gz

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S. cerevisiae Mub1, a substrate adaptor of E3 ubiquitin ligase, modulates sensitivity to cell wall stressors through multiple transcription factors

Project description:Yeasts evolved a complex regulatory program to build and maintain their cell wall, the primary structure through which they interact with their environment. However, how this program ties to essential cellular processes mostly remains unclear. Here, we focus on Saccharomyces cerevisiae Mub1, an adaptor protein of E3 ubiquitin ligase Ubr2, previously associated with regulating proteasome genes through transcription factor Rpn4. We show that S. cerevisiae cells lacking Mub1 become hyper-tolerant to standard cell wall stressors, outperforming wild-type cells. This protective mub1Δ phenotype stems from the activity of several transcription factors, leading to the inhibition of cell wall remodelling, a typically protective process that becomes maladaptive during chronic cell wall stress in laboratory conditions. Based on these results, we suggest Mub1 regulates not only Rpn4 but a much broader range of transcription factors and thus serves as an in-so-far unrecognised regulatory hub directly linking cell wall robustness with the ubiquitin-proteasome system.

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E3 ligase substrate adaptor SPOP fine tunes the UPR of pancreatic beta cells

Project description:The Cullin-3 E3 ligase adaptor protein, SPOP, targets proteins for ubiquitination and proteasomal degradation. We previously established the β cell transcription factor (TF) and human diabetes gene PDX1 as an SPOP substrate, suggesting a functional role for SPOP in the β cell. Here, we generated a β cell specific Spop deletion mouse strain (SpopβKO) and found that Spop is necessary to prevent aberrant basal insulin secretion and for maintaining glucose- stimulated insulin secretion (GSIS) through impacts on glycolysis and glucose-stimulated calcium flux. Integration of proteomic, TF-regulatory gene network and biochemical analyses identified XBP1 as a functionally important SPOP substrate in pancreatic β cells. Further, loss of SPOP strengthened the IRE1α-XBP1 axis of unfolded protein response (UPR) signaling. ER stress promoted proteasomal degradation of SPOP, supporting a model whereby SPOP fine-tunes XBP1 activation during the UPR. These results position SPOP as a regulator of β cell function and proper UPR activation.

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E3 ligase substrate adaptor SPOP fine tunes the UPR of pancreatic beta cells

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The AMBRA1 E3 ligase adaptor regulates Cyclin D protein stability

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Project description:Clonal hematopoiesis is a prevalent age-related condition associated with greatly increased risk of hematologic malignancies. Mutations in DNA methyltransferase 3A (DNMT3A) are the most common drivers of this state and contribute to multiple types of hematologic malignancy. DNMT3A variants occur across the gene and some are associated with particular disease states, but the functional relevance and mechanisms of pathogenesis of the majority of the mutations is unknown. Here, we systematically investigated the methyltransferase activity and protein stability of 253 disease-associated DNMT3A mutations, finding that 74% were loss-of-function mutations. Nearly half of these variants exhibited reduced protein stability and, as a class, correlated with greater clonal expansion and AML development. To identify the mechanisms underlying the instability, we conducted a CRISPR screen and uncovered regulated destruction of DNMT3A mediated by the DCAF8 E3 ubiquitin ligase adaptor. We establish a new paradigm to classify novel variants that has prognostic and therapeutic significance for patients with hematologic disease.

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β-arrestin1 is an E3 ubiquitin ligase adaptor for substrate linear polyubiquitination.

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