Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SIRT6 maintains redox homeostasis to promote porcine oocyte maturation

ABSTRACT: SIRT6 maintains redox homeostasis to promote porcine oocyte maturation

PROVIDER: PRJNA675479 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13009985_1.fastq.gz	Fastqsanger.gz
	SRR13009985_2.fastq.gz	Fastqsanger.gz
	SRR13009986_1.fastq.gz	Fastqsanger.gz
	SRR13009986_2.fastq.gz	Fastqsanger.gz
	SRR13009987_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

SIRT6 maintains redox homeostasis to promote porcine oocyte maturation

Project description:SIRT6, the sixth member of sirtuin family proteins, has been identified as a crucial regulator in multiple molecular pathways related to aging, including genome stability, DNA damage repair, telomere maintenance and inflammation. However, the exact roles of SIRT6 during mammalian oocyte meiosis have not yet fully clarified. Here, we investigated the critical events during porcine oocyte meiotic maturation with the treatment of SIRT6 specific inhibitor SIRT6-IN-1. We found that SIRT6 inhibition resulted in oocyte meiotic failure by displaying the poor expansion of cumulus cells and reduced rate of polar body extrusion. Meanwhile, the compromised spindle assembly, chromosome alignment and actin dynamics were also observed in SIRT6-inhibited oocytes. Moreover, inhibition of SIRT6 led to the defective cytoplasmic maturation by showing the abnormal distribution of cortical granules and their component ovastacin. Notably, we identified that expression of genes related to oocyte meiosis, oxidative phosphorylation and cellular senescence was remarkably altered in SIRT6-inhibited oocytes by transcriptome analysis, and validated that the meiotic defects caused by SIRT6 inhibition resulted from the excessive ROS-induced early apoptosis in oocytes. Taken together, our findings demonstrate that SIRT6 promotes the porcine oocyte meiotic maturation via maintaining the organelle dynamics.

2021-03-16 | GSE161068 | GEO

SIRT6 Maintains Redox Homeostasis to Promote Porcine Oocyte Maturation.

Project description:SIRT6, the sixth member of the sirtuin family proteins, has been characterized as a crucial regulator in multiple molecular pathways related to aging, including genome stability, DNA damage repair, telomere maintenance, and inflammation. However, the exact roles of SIRT6 during female germ cell development have not yet been fully determined. Here, we assessed the acquisition of meiotic competency of porcine oocytes by inhibition of SIRT6 activity. We observed that SIRT6 inhibition led to the oocyte meiotic defects by showing the impairment of polar body extrusion and cumulus cell expansion. Meanwhile, the compromised spindle/chromosome structure and actin dynamics were also present in SIRT6-inhibited oocytes. Moreover, SIRT6 inhibition resulted in the defective cytoplasmic maturation by displaying the disturbed distribution dynamics of cortical granules and their content ovastacin. Notably, we identified that transcript levels of genes related to oocyte meiosis, oxidative phosphorylation, and cellular senescence were remarkably altered in SIRT6-inhibited oocytes by transcriptome analysis and validated that the meiotic defects caused by SIRT6 inhibition might result from the excessive reactive oxygen species (ROS)-induced early apoptosis in oocytes. Taken together, our findings demonstrate that SIRT6 promotes the porcine oocyte meiotic maturation through maintaining the redox homeostasis.

| S-EPMC7947247 | biostudies-literature

SIRT6 regulates redox homeostasis in human mesenchymal stem cells by the transactivation of NRF2

Project description:We investigated the effect of SIRT6-knockout on gene expression and H3K4me3 modification profile in human mesenchymal stem cells. RNAs isolated from SIRT6+/+ and SIRT6-/- hMSCs at early and late passages were sequenced, respectively. And, H3K4me3 ChIP-seq was performed upon the SIRT6 deleted hMSC and WT at early stage, respectively.

2016-01-04 | E-GEOD-64642 | biostudies-arrayexpress

CPEB3 Maintains Developmental Competence of the Oocyte

Project description:CPEB3 Maintains Developmental Competence of the Oocyte

| PRJNA999673 | ENA

Endo-siRNAs repress expression of SINE1B during in vitro maturation of porcine oocyte

Project description:We performed small RNA-seq on Dicer KD and control porcine oocyte, and report endo-siRNAs corresponding to SINE1B are significantly down-regulated by Dicer knockdown and are essential for in vitro maturation of porcine oocyte

2018-12-04 | GSE123274 | GEO

Sirt6 study

Project description:This SuperSeries is composed of the following subset Series: GSE13206: Human shSIRT6 TNF-alpha timecourse GSE13207: Mouse Sirt6-/- TNF-alpha timecourse GSE13208: Mouse Sirt6-/- tissues GSE13209: Mouse Sirt6-/- RelA+/- tissues Refer to individual Series

2010-06-24 | E-GEOD-13272 | biostudies-arrayexpress

Selective autophagic degradation of ATP citrate lyase maintains citrate homeostasis and promotes oocyte maturation

Project description:Autophagy is a cellular and energy homeostatic mechanism that contributes to maintain the number of primordial follicles, germ cell survival, and anti-ovarian aging. However, it remains unknown whether autophagy in granulosa cells affects the oocyte maturation. Here, we show a clear tendency of reduced autophagy level in human granulosa cell from women of advanced maternal age, implying a potential negative correlation between autophagy level and oocyte quality. We therefore established a co-culture system and show that either pharmacological inhibition or genetic ablation of autophagy in granulosa cells negatively affect the oocyte quality and fertilization ability. Moreover, our metabolomics analysis indicates that the adverse impact of autophagy impairment on oocyte quality is mediated by downregulated citrate levels, while exogenous supplementation of citrate can significantly restore the oocyte maturation. In molecular level, we found ATP citrate lyase (Acly), which is a crucial enzyme catalyzing the cleavage of citrate, was preferentially associated with K63-linked ubiquitin chains and recognized by the autophagy receptor protein SQSTM1/p62 for the selective autophagic degradation. In human follicles, autophagy levels in granulosa cells was downregulated with maternal aging, accompanied by decreased citrate in the follicular fluid, implying a potential correlation between citrate metabolism and oocyte quality. We also show that elevated citrate levels in porcine follicular fluid promote oocyte maturation. Collectively, our data reveal that autophagy in granulosa cells is a beneficial mechanism to maintain a certain degree of citrate by selectively targeting Acly during oocyte maturation.

2023-01-09 | GSE190697 | GEO

Zebrafish oocyte maturation

Project description:The sequences deposited within this study are for the analysis of the changing transcriptome during zebrafish oocyte maturation. This dataset will be used to study the differential expression of mRNAs during oocyte maturation and also mechanisms of RNA stability and degradation, transcription and polyadenylation. Sequences will be generated using polyA selection and then, after reverse transcription, generated into illumina libraries. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2014-09-09 | E-ERAD-212 | biostudies-arrayexpress

HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge [oocyte-transcriptome]

Project description:HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge [oocyte-transcriptome]

| PRJNA586845 | ENA

SIRT6 regulates redox homeostasis in human mesenchymal stem cells by the transactivation of NRF2

Project description:We investigated the effect of SIRT6-knockout on gene expression and H3K4me3 modification profile in human mesenchymal stem cells.

2016-01-04 | GSE64642 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data