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Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE128843 | GEO | 2019/09/30

REPOSITORIES: GEO

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Mitofusin 2 plays a role in oocyte and follicle development, and is required to maintain ovarian follicular reserve during reproductive aging.

Project description:Mitochondria change their shape through fusion and fission in order to adapt to their metabolic milieu. Mitofusin-2 (MFN2) is a key regulatory protein in this process, mediating mitochondrial fusion and interaction with endoplasmic reticulum. Targeted deletion of Mfn2 in oocytes resulted in mitochondrial dysfunction and female subfertility associated with impaired oocyte maturation and follicle development. Oocytes lacking MFN2 showed shortened telomeres and increased apoptosis, resulting in compromised oocyte quality and accelerated follicular depletion, consistent with a reproductive aging phenotype.

| S-EPMC6628992 | biostudies-literature

Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [GV]

Project description:We performed RNAseq analysis to determine the effect of MFN2 deletion on oocyte global gene expression profile. RNAseq revealed a total of 363 genes were significantly differentially expressed (p<0.05) in Mfn2-/- GV oocytes compared to WT (241 up-regulated and 122 down-regulated). Gene ontology (GO) analysis indicated significant over-representation of elements involved in regulation of embryonic development, cell death and survival, and cell morphology. Pathway analysis of top10 upregulated and downregulated annotated genes are listed. Our findings provide new insight into the role of MFN2 in the oocytes, and may help understand the potential mechanism of subfertility and reproductive aging associated with MFN2-deficiency.

2019-09-30 | GSE128780 | GEO

Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [SFO]

Project description:We performed RNAseq analysis to determine the effect of MFN2 deletion on oocyte global gene expression profile. RNAseq revealed a total of 1041 genes were significantly differentially expressed (p<0.05) in Mfn2-/- seceondary follicle enclosed oocytes (SFOs) compared to WT, with 510 up-regulated and 531 down-regulated genes. GO cluster analysis indicated significant over-representation of elements involved in regulation of cell death and survival, cellular development and cellular growth. Pathway analysis of top10 upregulated and downregulated annotated genes are listed. Our findings provide new insight into the role of MFN2 in the oocytes, and may help understand the potential mechanism of subfertility and reproductive aging associated with MFN2-deficiency.

2019-09-30 | GSE128808 | GEO

Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging

Project description:Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging

| PRJNA529060 | ENA

Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [GV]

Project description:Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [GV]

| PRJNA528880 | ENA

Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [SFO]

Project description:Mitofusin 2 is essential for oocyte and follicle development, and to maintain ovarian follicular reserve during reproductive aging [SFO]

| PRJNA528927 | ENA

Mitofusin 1 is required for female fertility and to maintain ovarian follicular reserve.

Project description:Mitochondria are dynamic organelles that continually adapt their structure through fusion and fission in response to changes in their bioenergetic environment. Targeted deletion of mitochondrial fusion protein mitofusin1 (MFN1) in oocytes resulted in female infertility associated with failure to achieve oocyte maturation. Oocyte-granulosa cell communication was impaired, and cadherins and connexins were downregulated, resulting in follicle developmental arrest at the secondary follicle stage. Deletion of MFN1 in oocytes resulted in mitochondrial dysfunction and altered mitochondrial dynamics, as well as accumulation of ceramide, which contributed to increased apoptosis and a reproductive phenotype that was partially rescued by treatment with ceramide synthesis inhibitor myriocin. Absence of MFN1 and resulting apoptotic cell loss also caused depletion of ovarian follicular reserve, and a phenotype consistent with accelerated female reproductive aging.

| S-EPMC6646343 | biostudies-literature

Mitochondrial unfolded protein response gene Clpp is required to maintain ovarian follicular reserve during aging, for oocyte competence, and development of pre-implantation embryos.

Project description:Caseinolytic peptidase P mediates degradation of unfolded mitochondrial proteins and activates mitochondrial unfolded protein response (mtUPR) to maintain protein homeostasis. Clpp-/- female mice generate a lower number of mature oocytes and two-cell embryos, and no blastocysts. Clpp-/- oocytes have smaller mitochondria, with lower aspect ratio (length/width), and decreased expression of genes that promote fusion. A 4-fold increase in atretic follicles at 3 months, and reduced number of primordial follicles at 6-12 months are observed in Clpp-/- ovaries. This is associated with upregulation of p-S6, p-S6K, p-4EBP1 and p-AKT473, p-mTOR2481 consistent with mTORC1 and mTORC2 activation, respectively, and Clpp-/- oocyte competence is partially rescued by mTOR inhibitor rapamycin. Our findings demonstrate that CLPP is required for oocyte and embryo development and oocyte mitochondrial function and dynamics. Absence of CLPP results in mTOR pathway activation, and accelerated depletion of ovarian follicular reserve.

| S-EPMC6052477 | biostudies-other

Reproductive Longevity and Aging: Geroscience Approaches to Maintain Long-Term Ovarian Fitness.

Project description:Increases in delayed childbearing worldwide have elicited the need for a better understanding of the biological underpinnings and implications of age-related infertility. In women 35 years and older the incidences of infertility, aneuploidy, and birth defects dramatically increase. These outcomes are a result of age-related declines in both ovarian reserve and oocyte quality. In addition to waning reproductive function, the decline in estrogen secretion at menopause contributes to multisystem aging and the initiation of frailty. Both reproductive and hormonal ovarian function are limited by the primordial follicle pool, which is established in utero and declines irreversibly until menopause. Because ovarian function is dependent on the primordial follicle pool, an understanding of the mechanisms that regulate follicular growth and maintenance of the primordial follicle pool is critical for the development of interventions to prolong the reproductive life span. Multiple pathways related to aging and nutrient-sensing converge in the mammalian ovary to regulate quiescence or activation of primordial follicles. The PI3K/PTEN/AKT/FOXO3 and associated TSC/mTOR pathways are central to the regulation of the primordial follicle pool; however, aging-associated systems such as the insulin-like growth factor-1/growth hormone pathway, and transsulfuration/hydrogen sulfide pathways may also play a role. Additionally, sirtuins aid in maintaining developmental metabolic competence and chromosomal integrity of the oocyte. Here we review the pathways that regulate ovarian reserve and oocyte quality, and discuss geroscience interventions that leverage our understanding of these pathways to promote reproductive longevity.

| S-EPMC8361335 | biostudies-literature

Size-specific follicle selection improves mouse oocyte reproductive outcomes.

Project description:Encapsulated in vitro follicle growth (eIVFG) has great potential to provide an additional fertility preservation option for young women and girls with cancer or other reproductive health threatening diseases. Currently, follicles are cultured for a defined period of time and analyzed as a cohort. However, follicle growth is not synchronous, and culturing follicles for insufficient or excessive times can result in compromised gamete quality. Our objective is to determine whether the selection of follicles based on size, rather than absolute culture time, better predict follicle maturity and oocyte quality. Multilayer secondary mouse follicles were isolated and encapsulated in 0.25% alginate. Follicles were cultured individually either for defined time periods or up to specific follicle diameter ranges, at which point several reproductive endpoints were analyzed. The metaphase II (MII) percentage after oocyte maturation on day 6 was the highest (85%) when follicles were cultured for specific days. However, if follicles were cultured to a terminal diameter of 300-350 ?m irrespective of absolute time in culture, 93% of the oocytes reached MII. More than 90% of MII oocytes matured from follicles with diameters of 300-350 ?m showed normal spindle morphology and chromosome alignment, 85% of oocytes showed two pronuclei after IVF, 81% developed into the two-cell embryo stage and 38% developed to the blastocyst stage, all significantly higher than the percentages in the other follicle size groups. Our study demonstrates that size-specific follicle selection can be used as a non-invasive marker to identify high-quality oocytes and improve reproductive outcomes during eIVFG.

| S-EPMC4527888 | biostudies-literature

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