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Posted

As you know, a person of age 29 should be able to create cell through meiosis that is of age 29 identical to the original cell, the cell does not become younger or older. However, sperm created through mitosis combines with egg to form a zygote of age 0. If the DNA damage theory is true that our cells DNA are damaged as we grow old, how come the sperm's DNA is not damaged, did we do a perfect repair on sperm's DNA to bring it back to age 0?

Posted

As you know, a person of age 29 should be able to create cell through meiosis that is of age 29 identical to the original cell, the cell does not become younger or older. However, sperm created through mitosis combines with egg to form a zygote of age 0. If the DNA damage theory is true that our cells DNA are damaged as we grow old, how come the sperm's DNA is not damaged, did we do a perfect repair on sperm's DNA to bring it back to age 0?

I think the defective parts in the spermazoa can be negated, somewhat, when it combines with an ovum, since it only contributes 50% of the genes to the foetus. If the combination is an xx result then then the probability of it negating any defects increases because there is a greater likely of this occurring due to there are two copies of x in a female mate and female progeny. I think this is one of the reasons why females are more robust genetically and live longer. The spermazoa's age is zero. If you clone a cell then the progeny will be the age of the parents.

Posted (edited)

My speculation is following the DNA damage theory that the cell gets damaged over time as it ages. Following this theory, the sperm cell created through mitosis either does a perfect repair or the DNA damage theory is wrong in which the DNA damage is not the cause for aging and the sperm's gene expression is being reset. Again the cause for aging is still unknown, but the sperm created through mitosis cannot have defective genes

 

P.S. Well, we've never really examined the DNA in sperm have we?

Edited by fredreload
Posted (edited)

Competition between sperm helps to weed out defects.

 

The repair mechanisms can themselves be damaged. Main problem that evolution had to find a way around.

 

Telomere shortening plays a role in aging as well. Necessarily any reproductive cells(along with a few others) are reset in that sense.

Edited by Endy0816
Posted (edited)

It is really based on logic reasoning. Well, let it be Telomere or other DNA strands, whichever gets reset during the mitosis process might be the key to aging. There really shouldn't be any DNA damage on the sperm cells, if the amount of damage equals to the number of ages of a person, a damaged sperm could give rise to a 5, 10 years old, which is impossible. So somewhere along the line there should be a perfect reset, let it be lengthening the Telomere or repair the gene damages, clearly something is able to reset the damage to DNA.

 

Short reasoning:

Damage to my DNA causing me to age to 29 years old -> Create damaged DNA sperms -> Sperm give rise to 29 years old baby is clearly impossible

 

P.S. Endy0816, you are right, Telomere does sounds like the key to aging

Edited by fredreload
Posted

The spermatocytic DNA is not always perfect, there can be sporadic mutations that develop in individual sperm cells as a result of imperfect DNA repair.

 

I learned it on this forum too, but there is a genetic condition called Smith-Magenis Syndrome that develops due to sporadic mutations in sperm or ovum or early zygote. There is a thread about it on this forum.

 

https://ghr.nlm.nih.gov/condition/smith-magenis-syndrome

Posted

Well, DNA should be pretty accurate in doing the tasks = =, I'm saying this for normal conditions, but you know, the answer is in the mitosis stage, Telomere sounds pretty fishy

Posted

My speculation is...

 

!

Moderator Note

Moved to Speculations. We need to keep non-mainstream ideas separate so students aren't misinformed.

 

Please support your ideas with as much evidence as you can.

Posted

Also, chromosomal disorders like Down's, Turner's, Klinefelter's, as well as diseases of genomic imprinting like Prader-Willi, Angelman's syndrome almost always develop sporadically during meiosis and spermatogenesis.

Posted (edited)

Well again, I'm saying it for normal condition of mitosis and if Telomere is repaired during this process

Spermatogenesis is a meiotic, not mitotic, process.

 

Mitosis

Mitosis is used to produce daughter cells that are genetically identical to the parent cells. The cell copies - or 'replicates' - its chromosomes, and then splits the copied chromosomes equally to make sure that each daughter cell has a full set.

 

Meiosis Meiosis is used to make special cells - sperm cells and egg cells - that have half the normal number of chromosomes. It reduces the number from 23 pairs of chromosomes to 23 single chromosomes. The cell copies its chromosomes, but then separates the 23 pairs to ensure that each daughter cell has only one copy of each chromosome. A second division that divides each daughter cell again to produce four daughter cells.

http://www2.le.ac.uk/departments/genetics/vgec/highereducation/topics/cellcycle-mitosis-meiosis

 

 

 

Edited by StringJunky
Posted

Right, thanks for the correction on meiosis. Well, technically all we have to do is to open a few of these sperm cells and check the length of the Telomere as well as if the damaged DNA has been repaired to its initial state. I don't think adding a part of Telomere length DNA to every single cell at my current age 29 is going to help me live longer, there's probably other things at work here (DNA damage). Although I can imagine growing into a younger age 29->28->27. Then again if all meiosis does is a perfect reset that wouldn't quite work out either, no one wants to be a zygote age 29->0. Well, so all we need is to open a few of these sperm packages

Posted (edited)

I believe the article you posted is referring to mutation, please check the distinction between DNA damage and mutation here.

 

Wikipedia: "DNA damage is any physical abnormality in the DNA, such as single and double strand breaks, 8-hydroxydeoxyguanosine residues and polycyclic aromatic hydrocarbon adducts."

Edited by fredreload

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