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Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

ABSTRACT: Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

PROVIDER: PRJNA1111379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29016173_1.fastq.gz	Fastqsanger.gz
	SRR29016173_2.fastq.gz	Fastqsanger.gz

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Uchl1 maintains energy and metabolic homeostatic balance during spermatogenesis

Project description:In mammals, spermatogenesis plays a critical role in upholding the genetic stability of the male germline; however, disruptions such as viral and bacterial infections, toxic damage, genetic mutations, or deletions can disturb the delicate equilibrium of the testicular microenvironment, ultimately resulting in impaired spermatogenesis and male infertility. One key protein involved in this process is UCHL1, which possesses deubiquitinating enzyme, multiple ligases, and hydrolase activities. In addition to its roles in maintaining neuronal activity and memory function in the brain, UCHL1 is also implicated in spermatogenesis. Nevertheless, the precise mechanism by which it sustains metabolic homeostasis during spermatogenesis remains unclear. To investigate this, we generated Uchl1_KO mice and subjected their testes to snRNA-seq and metabolomics sequencing. Our analysis revealed that Uchl1_KO mice exhibited abnormal spermatogenesis, decreased testicular OXHPOS levels, and disrupted ADIPONECTIN signaling, concomitant with heightened inflammatory signaling and disturbances in lipid metabolism and energy homeostasis in the testes. These findings suggest that Uchl1 plays a crucial role in spermatogenesis by modulating energy and metabolic pathways within the testes to maintain orderly spermatogenesis. This study contributes to the understanding of the energy and metabolic balance required for successful male spermatogenesis.

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Metabolic reprogramming in astrocytes prevents neuronal death through a UCHL1/PFKFB3/H4K8la positive feedback loop

Project description:Astrocytic metabolic reprogramming is an adaptation of metabolic patterns to meet increased energy demands, although the role after spinal cord injury (SCI) remains unclear. Analysis of single-cell RNA sequencing (scRNA-seq) data identified an increase in astrocytic glycolysis, while PFKFB3, a key regulator of glycolytic flux, was significantly upregulated following SCI. Loss of PFKFB3 in astrocytes prohibited neuronal energy supply and enhanced neuronal ferroptosis in vitro and inhibited astrogliosis, expanded neuroinflammation, exacerbated neuronal loss, and hindered functional recovery in vivo after SCI. Mechanistically, deubiquitinase UCHL1 plays a crucial role in stabilizing and enhancing PFKFB3 expression by cleaving K48-linked ubiquitin chains. Genetic deletion of Uchl1 inhibited locomotor recovery after SCI by suppression of PFKFB3-induced glycolytic reprogramming in astrocytes. Furthermore, the UCHL1/PFKFB3 axis increased lactate production, leading to enhanced histone lactylation and subsequent transcription of Uchl1 and several genes related to glycolysis, suggesting a glycolysis/H4K8la/UCHL1 positive feedback loop. These findings help to clarify the role of the UCHL1/PFKFB3/H4K8la loop in modulation of astrocytic metabolic reprogramming and reveal a potential target for treatment of SCI.

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Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1 UCHL1 was knocked down in A2780 (A2780-shUCHL1). A2780-shUCHL1 and A2780-control were cultured in RPMI and total RNA was extracted and hybridizated on Affymetrix.GeneChip.HG-U133_Plus_2

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