Dataset Information

Profiling postnatal folliculogenesis in ovaries with loss of oocyte SUMOylation

ABSTRACT: SUMOylation plays a critical role in regulating protein function. In the ovary, disrupting expression of the E2 SUMO conjugation enzyme in mouse oocytes beginning at the primordial follicle stage results in female sterility and loss of the ovarian reserve in early adulthood. To determine how folliculogenesis is disrupted, we used label-free mass spectrometry to profile day 14 control and Ube2i-Gdf9icre ovaries.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Oocyte

SUBMITTER: Antrix Jain

LAB HEAD: Stephanie A. Pangas

PROVIDER: PXD055913 | Pride | 2025-05-07

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	33225_1_00F_Ooocyte_WT1_1ug_0625.msf	Msf
	33225_1_00F_Ooocyte_WT1_1ug_0625.raw	Raw
	33225_1_00F_Ooocyte_WT1_1ug_0930.msf	Msf
	33225_1_00F_Ooocyte_WT1_1ug_0930.raw	Raw
	33225_1_00F_Ooocyte_WT1_1ug_1235.msf	Msf

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Publications

Disruption of oocyte SUMOylation impacts critical regulatory processes during folliculogenesis in mice†.

Liao Zian Z Steenwinkel Tessa E TE Moscoso Bruno B Salas Ernesto E Patton Bethany K BK Rodriguez Amanda A Malovannaya Anna A Pangas Stephanie A SA

Biology of reproduction 20250501 5

The conjugation of small ubiquitin-like modifiers (SUMO) to target proteins, known as SUMOylation, plays a crucial role in regulating protein homeostasis, activity, interaction with other proteins, and subcellular localization. Loss of SUMOylation in nongrowing oocytes by conditional deletion of the E2 SUMO conjugating enzyme, Ube2i, at the primordial follicle stage leads to female sterility due to complex changes in oocyte development, including altered folliculogenesis, defective meiotic progr ...[more]

PMID: 39982420

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Project description:The oocytes found within the primordial follicles of mammalian ovaries remain quiescent for months to years until they receive the appropriate signals to undergo the primordial to primary follicle transition and initiate folliculogenesis. The molecular mechanisms and extracellular signaling factors that regulate this process remain to be fully elucidated. The current study investigates the mechanisms utilized by anti-MÃ¼llerian hormone (AMH; i.e. MÃ¼llerian inhibitory substance) to inhibit the primordial to primary follicle transition. Ovaries from 4-day-old rats were placed into organ culture and incubated in the absence or presence of AMH, either alone or in combination with known stimulators of follicle transition, including basic fibroblast growth factor (bFGF), kit ligand (KITL), or keratinocyte growth factor (KGF). Following 10 days of culture, the ovaries were sectioned, stained, and morphologically evaluated to determine the percentage of primordial versus developing follicles. As previously demonstrated, AMH treatment decreased primordial to primary follicle transition. Interestingly, AMH inhibited the stimulatory actions of KITL, bFGF, and KGF. Therefore, AMH can inhibit the basal and stimulated development of primordial follicles. To investigate the mechanism of AMH actions, the influence AMH has on the ovarian transcriptome was analyzed. AMH treatment when compared with controls was found to alter the expression of 707 genes. The overall effect of AMH exposure is to decrease the expression of stimulatory factors, increase the expression of inhibitory factors, and regulate cellular pathways (e.g. transforming growth factor beta signaling pathway) that result in the inhibition of primordial follicle development. Analysis of the regulatory factors and cellular pathways altered by AMH provides a better understanding of the molecular control of primordial follicle development. Experiment Overall Design: RNA samples from two control groups (pooled untreated cultured ovaries) are compared to two treated groups (pooled cultured ovaries treated with AMH)