Poster Session 5, 3:15 PM - 4:00 PM: Room 163 [C23]

Functional Analysis of SUGT1 During Mouse Oocyte Development

Presenter: Hsin Lee

Faculty Sponsor: Wei Cui

School: UMass Amherst

Research Area: Animal Science

ABSTRACT

Sugt1 (also known as Sgt1) is an essential protein-coding gene that participates in multiple fundamental cellular processes, including ubiquitination, proteasomal degradation, kinetochore assembly, centrosome maturation, and protein homeostasis through its role as a co-chaperone of Hsp90. Conventional Sugt1 knockout results in early embryonic lethality in mice, making tissue-specific functions of this gene difficult to study. To investigate the role of Sugt1 during oocyte development, we established an oocyte-specific Sugt1 conditional knockout (cKO) model using the Cre/LoxP system driven by Gdf9-Cre to restrict deletion of Sugt1 to oocytes.

Oocytes are central to female reproduction and undergo a tightly regulated maturation process that is essential for generating developmentally competent eggs. Preliminary findings indicate that Sugt1 cKO females are functionally infertile under our experimental conditions. While no overt defects were observed in germinal vesicle (GV) oocytes with respect to oocyte number or gross morphology, metaphase II (MII) oocytes collected from the oviducts exhibited markedly reduced numbers, decreased survival rates, and pronounced morphological abnormalities. cKO oocytes frequently lacked a first polar body and showed abnormal microtubule organization and chromosome clustering, suggesting defects in meiotic progression.

Immunofluorescence analyses using markers for microtubules, apoptosis, DNA damage, and chromatin revealed clear structural differences between control and cKO oocytes. Based on these observations, we hypothesize that loss of Sugt1 in oocytes disrupts spindle and cytoskeletal organization, chromatin integrity, and chromosome separation required for successful oocyte maturation. This study aims to comprehensively phenotype MII oocyte abnormalities caused by Sugt1 deletion and to clarify the role of Sugt1 in mammalian oocyte development.

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