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后代的端粒长度由受精时的线粒体-细胞核通讯决定。

Telomere length in offspring is determined by mitochondrial-nuclear communication at fertilization.

作者信息

Winstanley Yasmyn E, Rose Ryan D, Sobinoff Alexander P, Wu Linda L, Adhikari Deepak, Zhang Qing-Hua, Wells Jadon K, Wong Lee H, Szeto Hazel H, Piltz Sandra G, Thomas Paul Q, Febbraio Mark A, Carroll John, Pickett Hilda A, Russell Darryl L, Robker Rebecca L

机构信息

Robinson Research Institute, School of Biomedicine, The University of Adelaide, Adelaide, SA, Australia.

Genea Fertility SA, St. Andrews Hospital, Adelaide, SA, Australia.

出版信息

Nat Commun. 2025 Mar 14;16(1):2527. doi: 10.1038/s41467-025-57794-7.

DOI:10.1038/s41467-025-57794-7
PMID:40087268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11909127/
Abstract

The initial setting of telomere length during early life in each individual has a major influence on lifetime risk of aging-associated diseases; however there is limited knowledge of biological signals that regulate inheritance of telomere length, and whether it is modifiable is not known. We now show that when mitochondrial activity is disrupted in mouse zygotes, via exposure to 20% O or rotenone, telomere elongation between the 8-cell and blastocyst stage is impaired, with shorter telomeres apparent in the pluripotent Inner Cell Mass (ICM) and persisting after organogenesis. Identical defects of elevated mtROS in zygotes followed by impaired telomere elongation, occurred with maternal obesity or advanced age. We further demonstrate that telomere elongation during ICM formation is controlled by mitochondrial-nuclear communication at fertilization. Using mitochondrially-targeted therapeutics (BGP-15, MitoQ, SS-31, metformin) we demonstrate that it is possible to modulate the preimplantation telomere resetting process and restore deficiencies in neonatal telomere length.

摘要

个体生命早期端粒长度的初始设定对与衰老相关疾病的终生风险有重大影响；然而，对于调节端粒长度遗传的生物信号了解有限，而且其是否可改变尚不清楚。我们现在表明，当通过暴露于20%氧气或鱼藤酮使小鼠受精卵中的线粒体活性受到干扰时，8细胞期和囊胚期之间的端粒延长会受损，在多能内细胞团（ICM）中可明显看到端粒更短，并且在器官发生后仍然存在。受精卵中mtROS升高继而端粒延长受损的相同缺陷，在母体肥胖或高龄时也会出现。我们进一步证明，ICM形成过程中的端粒延长是由受精时的线粒体-核通讯控制的。使用线粒体靶向治疗药物（BGP-15、MitoQ、SS-31、二甲双胍），我们证明有可能调节植入前端粒重置过程并恢复新生儿端粒长度的缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/e97d81e737a9/41467_2025_57794_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/72193c154156/41467_2025_57794_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/096b204d2ddf/41467_2025_57794_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/82292d51d764/41467_2025_57794_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/e78d1f18913a/41467_2025_57794_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/42dcdb20f7ec/41467_2025_57794_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/c3f5c038adef/41467_2025_57794_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/a983bb785eed/41467_2025_57794_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/f411f0276b6c/41467_2025_57794_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/e97d81e737a9/41467_2025_57794_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/72193c154156/41467_2025_57794_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/096b204d2ddf/41467_2025_57794_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/82292d51d764/41467_2025_57794_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/e78d1f18913a/41467_2025_57794_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/42dcdb20f7ec/41467_2025_57794_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/c3f5c038adef/41467_2025_57794_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/a983bb785eed/41467_2025_57794_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/f411f0276b6c/41467_2025_57794_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f442/11909127/e97d81e737a9/41467_2025_57794_Fig9_HTML.jpg

相似文献

[1]
Telomere length in offspring is determined by mitochondrial-nuclear communication at fertilization.

Nat Commun. 2025-3-14

[2]
Different telomere-length dynamics at the inner cell mass versus established embryonic stem (ES) cells.

Proc Natl Acad Sci U S A. 2011-8-24

[3]
Spermatozoa telomeres determine telomere length in early embryos and offspring.

Reproduction. 2016-1

[4]
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[5]
Mitochondrial dysfunction leads to telomere attrition and genomic instability.

Aging Cell. 2002-10

[6]
[Telomere lengthening by trichostatin A treatment in cloned pigs].

Yi Chuan. 2012-12

[7]
Telomere length determines the mitochondrial copy number in blastocyst-stage embryos.

Mitochondrion. 2024-7

[8]
Telomere Length in Metaphase Chromosomes of Human Triploid Zygotes.

Int J Mol Sci. 2021-5-25

[9]
Mitochondria-targeted therapy rescues development and quality of embryos derived from oocytes matured under oxidative stress conditions: a bovine in vitro model.

Hum Reprod. 2019-10-2

[10]
Resveratrol intake by males increased the mitochondrial DNA copy number and telomere length of blastocysts derived from aged mice.

J Reprod Dev. 2024-8-7

引用本文的文献

[1]
NAD-dependent Sirt6 is a key regulator involved in telomere shortening of in vitro-cultured preimplantation embryos.

Commun Biol. 2025-8-23

本文引用的文献

[1]
Familial Clonal Hematopoiesis in a Long Telomere Syndrome.

N Engl J Med. 2023-6-29

[2]
Leukocyte telomere length in children born following blastocyst-stage embryo transfer.

Nat Med. 2022-12

[3]
Genetics of human telomere biology disorders.

Nat Rev Genet. 2023-2

[4]
Female reproductive life span is extended by targeted removal of fibrotic collagen from the mouse ovary.

Sci Adv. 2022-6-17

[5]
Depletion of oocyte dynamin-related protein 1 shows maternal-effect abnormalities in embryonic development.

Sci Adv. 2022-6-17

[6]
Association of Telomere Length With Risk of Disease and Mortality.

JAMA Intern Med. 2022-3-1

[7]
Roles for the 8-Oxoguanine DNA Repair System in Protecting Telomeres From Oxidative Stress.

Front Cell Dev Biol. 2021-11-19

[8]
Epigenetic Reprogramming in Early Animal Development.

Cold Spring Harb Perspect Biol. 2022-6-14

[9]
Mitochondrial dysfunction and beneficial effects of mitochondria-targeted small peptide SS-31 in Diabetes Mellitus and Alzheimer's disease.

Pharmacol Res. 2021-9

[10]
Telomere dynamics across the early life course: Findings from a longitudinal study in children.

Psychoneuroendocrinology. 2021-7

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