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circMARK3 serves as a sponge of miR-205a to promote senescence of follicular granulosa cells in laying hens via regulating LIN9.

Created on 24 Oct 2026

Authors

Chi-Mei Liao, Yi-Meng Wei, Jia-Lin Xiang, Yi-Xuan Wang, Xin-Yue Zhao, Yao Zhang, Yu-Qi Chen, Hua-Dong Yin

Published in

Poultry science. Volume 105. Issue 12. Pages 107986. Oct 17, 2026. Epub Oct 17, 2026.

Abstract

Ovarian aging is a key factor contributing to the decline in reproductive performance of laying hens during the late laying period. A major contributor to ovarian aging is the accumulation of follicular senescence, and granulosa cell (GC) senescence is the molecular basis of follicular senescence. Circular RNAs (circRNAs) can act as competing endogenous RNAs (ceRNAs) by competitively binding microRNAs (miRNAs) and relieving their repression of downstream target genes. However, whether this ceRNA mechanism is involved in GC senescence in laying hens remains unclear. In earlier sequencing, circMARK3 expression was markedly increased in the ovarian follicles of laying hens during the late stage of egg production. Overexpression and knockdown of circMARK3 in primary GCs, combined with SA-β-gal staining, flow cytometry, and Western blotting, confirmed that circMARK3 promotes GC senescence in hens. Cellular fractionation and fluorescence in situ hybridization (FISH) confirmed that circMARK3 is predominantly localized in the cytoplasm, suggesting that it may function through a ceRNA mechanism. Bioinformatics prediction and dual-luciferase reporter assays indicated that circMARK3 directly binds miR-205a. Further experiments indicated that circMARK3 relieves miR-205a-mediated repression of Lin-9 homolog (LIN9), thereby upregulating LIN9 expression and ultimately promoting GC senescence. Collectively, these findings suggest that the circMARK3/miR-205a/LIN9 axis may be involved in GC senescence and follicular dysfunction in hens, providing a potential target for delaying ovarian aging in laying hens.

PMID:
42913217
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.

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