TCTP overexpression reverses age‐associated telomere attrition by upregulating telomerase activity in mouse oocytes

A prolonged time span between ovulation and fertilization can cause postovulatory aging of oocytes, which impairs oocyte quality and subsequent embryo development. Telomere attrition has long been considered as the primary hallmark of aging or the cause of age‐associated diseases. However, the statu...

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Bibliographic Details
Published in:Journal of cellular physiology 2022-01, Vol.237 (1), p.833-845
Main Authors: Jeon, Hyuk‐Joon, Kang, Minsung, Kim, Jae‐Sung, Oh, Jeong Su
Format: Article
Language:English
Subjects:
Age
Aging
Animals
BRCA1 protein
Chromosomes
Female
Fertilization
Gametocytes
Homology
Mice
oocyte
Oocytes
Oocytes - metabolism
Oogenesis
Ovulation
Oxidative stress
postovulatory aging
TCTP
Telomerase
Telomerase - genetics
Telomerase - metabolism
telomere
Telomere - genetics
Telomere - metabolism
Telomere Shortening
Telomeres
Tumor Protein, Translationally-Controlled 1 - metabolism
Tumors
Yeast
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Summary:A prolonged time span between ovulation and fertilization can cause postovulatory aging of oocytes, which impairs oocyte quality and subsequent embryo development. Telomere attrition has long been considered as the primary hallmark of aging or the cause of age‐associated diseases. However, the status of telomere and its regulation during postovulatory oocyte aging are poorly understood. Here we found that oocytes experience telomere shortening during postovulatory aging, although they have the capacity to maintain telomere length. However, translationally controlled tumor protein (TCTP) overexpression could reverse age‐associated telomere shortening by upregulating telomerase activity in mouse oocytes. Telomere length in mature oocytes gradually decreased with postovulatory aging, which was associated with a marked reduction in TRF1 expression, decreased telomerase activity, and decreased homologous combination (HR)‐based alternative lengthening of telomeres (ALT) with a concomitant increase in oxidative stress. Surprisingly, however, overexpression of TCTP led to a remarkable increase in telomere length during postovulatory aging. Notably, neither TRF1 nor BRCA1 level was altered by TCTP overexpression. Moreover, TCTP‐mediated telomere lengthening was not blocked by HR inhibition. In striking contrast, telomerase activity, as well as TERT and TERC levels, increased after TCTP overexpression. Importantly, unlike the chromosome‐wide distribution of endogenous TCTP, overexpressed TCTP was ectopically localized at telomeres, implying that TCTP overexpression is required to increase telomerase activity. Collectively, our results demonstrate that TCTP prevents telomere attrition during postovulatory aging by upregulating telomerase activity in mouse oocytes. Telomere length in mature oocytes gradually decreased with postovulatory aging with a marked reduction in TRF1 expression, decreased telomerase activity, and decreased homologous combination (HR)‐based alternative lengthening of telomeres (ALT) with a concomitant increase in oxidative stress. However, TCTP overexpression led to a remarkable increase in telomere length by upregulating telomerase activity in mouse oocytes.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.30557