https://www.reddit.com/r/askscience/comments/v4yvuk/why_are_babies_born_with_young_dna/
created by Enceing on 04/06/2022 at 21:47 UTC
12 upvotes, 4 top-level comments (showing 4)
[removed]
Comment by [deleted] at 05/06/2022 at 01:57 UTC*
20 upvotes, 1 direct replies
Only mutations in the germ cells (like sperm or eggs) are passed to offspring. Short telomeres and genomic instability in somatic cells do not affect the gametes or the offspring.
Much of the aging can be explained by problems in the epigenome i.e. modifications to DNA/chromatin which turn genes “on” and “off”. Most cells in your body have the same genome, but they have different functions and express different genes because of their epigenome (which genes are turned on and off). In a young person an eye cell only uses “eye cell genes”, a skin cell only uses “skin cell genes” and so on. But as you age the on and off signals gradually drift and your cells start to express too many of the wrong genes and not enough of the right ones and they don’t function as well (you get old). During development we go through a reset, where all of our cells are dedifferentiated (they are called totipotent stem cells) and then later differentiate into all the different cell types with the proper on and off switches.
Ultimately the baby has a shiny new epigenome (with some caveats as some things can be passed on) and they have the DNA from the gametes which hopefully have been fairly well protected with minimal mutations.
Edit: interestingly we can induce cells to differentiate into stem cells[1] and redifferentiate them again. This has even been done with cells take from 100 year olds and the result are healthy young cells[2], unfortunately doing this to a whole person rather than just a few cells would kill them so its not a cure for aging, just a demonstration that we can live longer.
1: https://en.m.wikipedia.org/wiki/Induced_pluripotent_stem_cell
2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219229/
Comment by palepinkpith at 05/06/2022 at 06:55 UTC*
13 upvotes, 0 direct replies
I'm a geneticist that studies age-acquired mutations.
The most important point here is that any mutation that occurs in the a tissue will be localized to that tissue, unless there is a cancer (e.g. mutations in a skin cell will only affect the skin). There isn't a mechanism to transfer that mutation to the gametes.
The chance of acquiring mutations is much higher during cell division. If you look at an aged body, tissues that have a high rate of cell division (e.g. skin, intestine) also have a higher mutational burden. Any age-related mutations will be contained to one tissue. So, mutations in the skin won't also be in the eggs or sperm.
But, since gametes are so important for the survival of our species, we evolved mechanisms to limit the frequency of mutations in gametes.
In females, all oocytes are produced while she is a fetus. Then they rest for her entire fertile life, with one being released and undergoing one round of meiosis for each menstrual cycle. So the number of times each egg cell has divided in the lifetime of her is extremely small. The oocytes are some of the least dividing cells in a womans body.
In men, Sperm precursors are regularly dividing to produce new sperm. The number of cell divisions that predated any sperm will be much higher than the egg. This is not great for the probability of acquiring mutations. This is why the father's age is a better predictor for autism, etc. than the mothers. That being said, sperm germ cells (precursors) have very low mutations rates. They spend a lot of their energy on DNA repair machinery and the population cooperates to 'take turns' in producing sperm. This way, they can limit the number of divisions any one germ cell makes. Sperm acquires about 2.9 new mutations every year.
Beyond the fact that new mutations are tissue/organ/locally specific, your point about wrinkles puts a little too much causation on DNA and mutations. DNA damage/mutations do not cause the majority of age-related changes. It is a complicated system of cell death, senescence, changes in hormones, endocrine production etc.
Comment by Vivid_Tamper at 05/06/2022 at 01:52 UTC
3 upvotes, 0 direct replies
The first cell is a stem cell, it starts to replicates more or less based on chemical hints of where it's situated and then after sufficient simple replications again based on there current location, cells gets locked into 1 type of cell (remaining DNA shuts off, appropriate part remains active).
That's why limbs doesn't grow from one's head (Generally).
Now these cells with locked DNA, do age, The ability to replicate slows down and at some point in time, they do not divide at all. Telomeres are the region of repetitive DNA at the end of chromosomes for DNA from tangling, Each time a cell divide, these telomeres keeps getting shorter.
Now the sole purpose of reproductive cells is to carry the information in DNA safe and secure, so these cells, likely can repeat the ends of chromosomes *increasing* the telomeres length in contrast to other cells.
The older the parents (still fertile), the younger the child, given the age solely depends on telomers length and gemot's telomers do get longer with the age.
Comment by Yithar at 05/06/2022 at 01:44 UTC*
2 upvotes, 1 direct replies
As for one thing that is associated with aging in humans, it's oxidative stress.
https://pubmed.ncbi.nlm.nih.gov/12882482/
Oxidative damage to DNA increases with age in several tissues and animal models, and mitochondrial DNA has a higher level of oxidative damage than nuclear DNA.
But also, male reproductive organs aren't necessarily immune to oxidative stress.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827380/
One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions.
But semen has special antioxidants that normally keep a balance with the Reactive Oxidative Species.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918773/
Sperm is particularly susceptible to reactive oxygen species (ROS) during critical phases of spermiogenesis. However, the level of seminal ROS is restricted by seminal antioxidants which have beneficial effects on sperm parameters and developmental potentials.