DYNLL1 transcript abundance decreases during oocyte and follicular growth and is associated with fertility in mice

Caglar Berkel , Ercan Cacan

Genome Instability & Disease ›› 2022, Vol. 4 ›› Issue (1) : 38 -45.

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Genome Instability & Disease ›› 2022, Vol. 4 ›› Issue (1) : 38 -45. DOI: 10.1007/s42764-022-00096-9
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DYNLL1 transcript abundance decreases during oocyte and follicular growth and is associated with fertility in mice

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Abstract

DNA repair efficiency is an important determinant of oocyte quality and female fertility. DYNLL1 (Dynein light chain 1) plays a part in DNA double-strand break (DSB) repair choice by promoting error-prone non-homologous end joining (NHEJ) repair and in contrast by limiting accurate and error-free homologous recombination (HR) repair. Here, we showed that DYNLL1 transcript abundance decreases gradually during oocyte and follicular growth in mice. In parallel, DYNLL1 mRNA transcript levels decline in the course of oocyte meiotic maturation in mice. Furthermore, our in silico analysis showed that ovaries from high-fertility mice with increased ovulation have lower DYNLL1 transcript abundance compared with that of control mice. Similarly, we found that the induction of ovulation with human chorionic gonadotropin (hCG) decreases DYNLL1 mRNA transcript levels in cumulus oocyte complexes in mice. We hypothesize that this decrease in DYNLL1 transcript abundance during oocyte and follicular growth and in ovulation might lead to relatively higher error-free HR repair and lower error-prone NHEJ repair events in mice, resulting in increased genome stability. Increased genome stability in mice with lower DYNLL1 levels might also contribute to better fertility performance. This paper highlights the need for further in vivo and mechanistic studies to better understand the role of DYNLL1 down-regulation in the maintenance of oocyte reserve and in oocyte quality and fertility.

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Caglar Berkel, Ercan Cacan. DYNLL1 transcript abundance decreases during oocyte and follicular growth and is associated with fertility in mice. Genome Instability & Disease, 2022, 4(1): 38-45 DOI:10.1007/s42764-022-00096-9

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Türkiye Bilimsel ve Teknolojik Araştırma Kurumu(2211-E)

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