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Developmental Biology - Gene Mutations

Fewer Gene Mutations May Predict Longer Life

The rate we acquire genetic mutations could help predict our lifespan and fertility...

Differences in the rate that genetic mutations accumulate in healthy young adults could help predict remaining lifespan in both sexes and the remaining years of fertility in women, according to University of Utah (U of U) Health scientists.
This study is believed to be the first of its kind that found young adults who acquired fewer mutations over time — lived about five years longer than those who acquire mutations more rapidly.

Researchers believe the discovery could eventually lead to the development of interventions to slow aging.
"If the results from this small study are validated by other independent research, it would have tremendous implications. It would mean we could possibly find ways to fix ourselves and live longer and better lives."

Lynn B. Jorde PhD, Chair, Department of Human Genetics, University of Utah; USTAR Center for Genetic Discovery, Salt Lake City, Utah, USA Health and co-author of the study.

The study appears online in the journal Nature: Scientific Reports.

Scientists have long known that DNA damage is constantly occurring in the body. Typically, various mechanisms repair this damage and prevent potentially harmful mutations, according to lead and corresponding author Richard Cawthon MD PhD, a U of U Health research associate professor of human genetics.
As we get older, body mechanisms become less efficient and more mutations accumulate. Older parents, for instance, tend to pass on more genetic mutations through their germline (egg or sperm) to their children than younger parents.

However, Cawthon and colleagues theorize that such mutations might be a useful biomarker for rates of aging, potentially predictive of lifespan in younger individuals — as well as fertility in women.

They then sequenced DNA from 61 men and 61 women grandparents in 41 three-generation families. The families were part of the Centre d'Etude du Polymorphisme Humain (CEPH) consortium, key to many investigations contributing to a modern understanding of human genetics.

This allowed for analysis of DNA in blood from pairs of grandparents in the first generation and compare it to one of their children in the second generation as germline (egg or sperm) mutations are passed to grandchildren. Mutations found in a child's blood not present in either parent's blood - are inferred to have originated from only that parents' egg or sperm. So scientists are now able to determine the number of these mutations each parent had accumulated in egg or sperm before conceiving their child. Knowing this allowed researchers to compare each first-generation parent to other first-generation parents of the same sex and be able to estimate their rate of aging.
"Compared to a 32-year-old man with 75 mutations, we would expect a 40-year-old with the same number of mutations to be aging more slowly. We'd expect him to die at an older age than the age at which the 32-year-old dies."

Richard M. Cawthon PhD, Department of Human Genetics, University of Utah, Salt Lake City, UT, USA.

Scientists found that mutations began to occur at an accelerating rate during or soon after puberty, suggesting that aging begins in our teens.Some young adults acquired mutations at up to three times the rate of others.
After adjusting for age, researchers determined individuals with the slowest rates of mutation accumulation were likely to live about five years longer than those who accumulated mutations more rapidly. This difference ia comparable to the effects of smoking - or lack of physical activity, Cawthon explains.

Women with the highest mutation rates had significantly fewer live births than other women and were more likely to be younger when they gave birth to their last child. This suggests that their high rate of mutation was affecting their fertility.

Richard Cawthon:"The ability to determine when aging starts, how long women can stay fertile, and how long people can live is exciting. If we can get to a point where we better understand what sort of developmental biology affects mutation rates during puberty, then we should be able to develop medical interventions to restore DNA repair and other homeostatic mechanisms back to what they were before puberty. If we could do that, it's possible people could live and stay healthy much longer."

Ageing may be due to mutation accumulation across the lifespan, leading to tissue dysfunction, disease, and death. We tested whether germline autosomal mutation rates in young adults predict their remaining survival, and, for women, their reproductive lifespans. Age-adjusted mutation rates (AAMRs) in 61 women and 61 men from the Utah CEPH (Centre d’Etude du Polymorphisme Humain) families were determined. Age at death, cause of death, all-site cancer incidence, and reproductive histories were provided by the Utah Population Database, Utah Cancer Registry, and Utah Genetic Reference Project. Higher AAMRs were significantly associated with higher all-cause mortality in both sexes combined. Subjects in the top quartile of AAMRs experienced more than twice the mortality of bottom quartile subjects (hazard ratio [HR], 2.07; 95% confidence interval [CI], 1.21–3.56; p = 0.008; median survival difference = 4.7 years). Fertility analyses were restricted to women whose age at last birth (ALB) was >= 30 years, the age when fertility begins to decline. Women with higher AAMRs had significantly fewer live births and a younger ALB. Adult germline mutation accumulation rates are established in adolescence, and later menarche in women is associated with delayed mutation accumulation. We conclude that germline mutation rates in healthy young adults may provide a measure of both reproductive and systemic ageing. Puberty may induce the establishment of adult mutation accumulation rates, just when DNA repair systems begin their lifelong decline.

Richard M. Cawthon, Huong D. Meeks, Thomas A. Sasani, Ken R. Smith, Richard A. Kerber, Elizabeth O’Brien, Lisa Baird, Melissa M. Dixon, Andreas P. Peiffer, Mark F. Leppert, Aaron R. Quinlan and Lynn B. Jorde.

The study was funded by the National Institutes of Health, the University of Utah Program in Personalized Health, the National Center for Research Resources, the National Center for Advancing Translational Sciences, the Howard Hughes Medical Institute, the W.M. Keck Foundation, and the George S. and Delores Doré Eccles Foundation.

The authors thank all the Utah individuals who participated in the CEPH consortium and all family members who participated in the UGRP. We thank Ray White, Ph.D. (deceased), and Jean-Marc Lalouel D.Sc., for their leadership in ascertaining and enrolling the Utah CEPH families in the 1980s to build the first comprehensive human genetic linkage map; and Stephen M. Prescott, M.D. for his leadership in envisioning and building the UGRP. We thank Alison M. Fraser, MSPH for conducting many queries of the UPDB. We thank Brent S. Pedersen, Ph.D. and Jeff Stevens for helpful discussions. This work was supported by NIH R01AG038797 and R21AG054962 (R.M.C.); University of Utah Program in Personalized Health (H.D.M.); NIH T32GM007464 (T.A.S.); NIH R01AG022095 (K.R.S.); NIH R01HG006693, R01HG009141, and R01GM124355 (A.R.Q.); NIH GM118335 and GM059290 (L.B.J.); NIH P30CA2014 (to the Utah Population Database, a.k.a. the UPDB); National Center for Research Resources Public Health Services grant M01RR00064 (to the Huntsman General Clinical Research Center, University of Utah); National Center for Advancing Translational Sciences NIH grant UL1TR002538 (to the University of Utah’s Center for Clinical and Translational Science); Howard Hughes Medical Institute funding (to Ray White); gifts from the W.M. Keck Foundation (to Stephen M. Prescott and M.F.L.) and from the George S. and Delores Doré Eccles Foundation (to the University of Utah) that supported the Utah Genetic Reference Project (UGRP). Sequencing of the CEPH samples was funded by the Utah Genome Project, the George S. and Dolores Doré Eccles Foundation, and the H.A. and Edna Benning Foundation. We thank the Pedigree and Population Resource of the Huntsman Cancer Institute, University of Utah (funded in part by the Huntsman Cancer Foundation) for its role in the ongoing collection, maintenance and support of the UPDB.

The authors declare no competing interests.

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Jul 1 2020   Fetal Timeline   Maternal Timeline   News

DNA mutations in blood from grandparents may pass to their child. And may also pass to grandchildren. Or, new mutations may rise solely in parents which they then pass on. Measuring these mutations in healthy young adults is possibly a way to measure that person's longevity as well as reproductive vitality. It may also give us clues to maximizing health.CREDIT Public Domain image.

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