sperm of age zero

[fredreload]

So as I've mentioned before. If the cell divide with mitosis, it would produce an identical cell at the same age. Just like I am age 30, so my cell would go through mitosis and produce an identical cell of age 30. Now here is my question about aging, when a cell goes through meiosis it produces cells with chromosomes that are halved known as gametes(sperm and egg). When sperm and egg combines, it produces a zygote which is of age zero (something that will turn into a baby). Now how does a human of age 30 produces sperm of age zero with meiosis? Some suggests that telomere is the key to aging, but when sperm is produced, is the telomere completely restored? I'm pretty sure normally there wouldn't be any defects to the babies, and humans doesn't give birth to a baby with shorter telomere, that means to reverse aging or to set the DNA back to its zero state is done in meiosis and all we have to do is to open a sperm and check its DNA to find out. If the sperm's DNA has a longer telomere, then we know it is restored in the meiosis process. If it is not, then something else might be at work.

Then there is the DNA damage theory, the DNA damage theory says that your DNA gets damaged as you grow older, but I think the zygote or babies can't possibly grow up with damaged DNA from the sperm, that means the DNA must also be repaired in the meiosis process. If the DNA is not repaired, then we know that DNA damage does not contribute to aging, all that matters is the telomere, or something else. I would like to know what you think Strange if you are reading this post

[Fuzzwood]

https://en.wikipedia.org/wiki/Telomerase

[fredreload]

https://en.wikipedia.org/wiki/Telomerase

Telomerase is only in theory. By checking the sperm cell wouldn't that confirm everything?

Edited August 10, 2016 by fredreload

[Strange]

Telomerase is only in theory. By checking the sperm cell wouldn't that confirm everything?

 

"Telomerase activity is extinguished during embryonic differentiation in most somatic cells but remains active in some tissues, such as male germ cells"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC120798/

 

"Telomerase activity was detected in fetal, newborn, and adult testes and ovaries, but not in mature spermatozoa or oocytes."

https://www.ncbi.nlm.nih.gov/pubmed/8934879

Telomerase is only in theory.

 

"Only in theory" ? You do know that "theory" is the strongest case science can make?

[fredreload]

 

"Telomerase activity is extinguished during embryonic differentiation in most somatic cells but remains active in some tissues, such as male germ cells"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC120798/

 

"Telomerase activity was detected in fetal, newborn, and adult testes and ovaries, but not in mature spermatozoa or oocytes."

https://www.ncbi.nlm.nih.gov/pubmed/8934879

 

"Only in theory" ? You do know that "theory" is the strongest case science can make?

Well then what really differs in a cell created through mitosis and the original cell? The cell created through mitosis is slightly bit older than the previous cell, possibly with some loss in telomere length. Does that mean all we need to do to get younger is by lengthening the telomere? What about the DNA damage theory?

 

P.S. Well, hook me up with one if you ever get it to work, counting on you

Edited August 10, 2016 by fredreload

[Endy0816]

Both play a role.

 

Telomeres help to keep DNA damage from being more of a problem for the organism as a whole. But the organism also needs replacement cells to keep on living.

[fredreload]

Well if meiosis is capable of fixing the damaged DNA, shouldn't we employ the same mechanism on our body? Or does each generation becomes more damaged then the previous generation?

[Endy0816]

Sex?

[fredreload]

Sex?

Well the way how meiosis repair DNA can also be used to repair normal cells if not reverse aging. Even if it does not there are still things we can learn from this mechanism toward reverse aging and immortality. I'm thinking DNA damage theory is not specific enough to cover everything at this point, still I respect the one that came up with the theory. I am not the guy who got a powerful enough microscope to observe DNA nor do I have a PHD in Biology degree. But this is a speculation forum, if you guys have any facts to challenge this idea feel free to bring it on

Edited August 12, 2016 by fredreload

[Endy0816]

 

Homologous recombination requires the presence of an identical or nearly identical sequence to be used as a template for repair of the break. The enzymatic machinery responsible for this repair process is nearly identical to the machinery responsible for chromosomal crossover during meiosis. This pathway allows a damaged chromosome to be repaired using a sister chromatid (available in G2 after DNA replication) or a homologous chromosome as a template. DSBs caused by the replication machinery attempting to synthesize across a single-strand break or unrepaired lesion cause collapse of the replication fork and are typically repaired by recombination.

 

https://en.wikipedia.org/wiki/DNA_repair

 

Related to telomeres and sperm:

 

http://blogs.discovermagazine.com/crux/2012/08/02/older-dads-give-good-telomeres-but-longevity-not-so-much/#.V66TtDUrvIU

 

Highlights the fact that there isn't a set length and that the repair ability remains limited. Basically trying to repair a blueprint with itself.

 

 

I find it interesting in general, the connection between the evolution of the double helix, lagging strand, shortening telomeres and eventually colonies of cells with different levels of repair capability.

 

As a colony of primarily cells lacking that ability, I think we should see about changing things up a bit.

 

 

Evidence that killing senescent cells improves lifespans.

 

http://www.sciencemag.org/news/2016/02/suicide-aging-cells-prolongs-life-span-mice

 

Coupled with introducing new cells with as few defects as possible, we may be able to increase this even more. Brain is probably the biggest issue. Introduced cells can and do(all-naturally) take up residence there though.

[fredreload]

 

https://en.wikipedia.org/wiki/DNA_repair

 

Related to telomeres and sperm:

 

http://blogs.discovermagazine.com/crux/2012/08/02/older-dads-give-good-telomeres-but-longevity-not-so-much/#.V66TtDUrvIU

 

Highlights the fact that there isn't a set length and that the repair ability remains limited. Basically trying to repair a blueprint with itself.

 

 

I find it interesting in general, the connection between the evolution of the double helix, lagging strand, shortening telomeres and eventually colonies of cells with different levels of repair capability.

 

As a colony of primarily cells lacking that ability, I think we should see about changing things up a bit.

 

 

Evidence that killing senescent cells improves lifespans.

 

http://www.sciencemag.org/news/2016/02/suicide-aging-cells-prolongs-life-span-mice

 

Coupled with introducing new cells with as few defects as possible, we may be able to increase this even more. Brain is probably the biggest issue. Introduced cells can and do(all-naturally) take up residence there though.

Well, I get DNA damage and repair, but does the same apply to sperm cells? Do sperm cells also get DNA damage before it is passed on for fertilization? I really don't think a zygote is formed with damaged sperm and damaged ovum, I could be wrong

 

P.S. How does the sperm and ovum remains undamaged? Could they survive a nuclear explosion?

Edited August 13, 2016 by fredreload

[Fuzzwood]

Sure, plenty of ovum and sperm cells that simply don't work. In any case, the DNA of sperm and ovum will differ slightly from that from the parent. If these mutations will be beneficial or detrimental to the new organism is up to the environment, enter evolution.

[fredreload]

Sure, plenty of ovum and sperm cells that simply don't work. In any case, the DNA of sperm and ovum will differ slightly from that from the parent. If these mutations will be beneficial or detrimental to the new organism is up to the environment, enter evolution.

Alright, but according to DNA damage theory, we age because our DNA is damaged. If the infants' DNA is damaged to begin with then they do not start out at age zero, a child could born old depending on how bad DNA damage is. Sure the infants' DNA might differ from the parent, but they can't be damaged

 

P.S. My idea is that sperm and ovum cannot be damaged, maybe they have an original copy of the DNA, the non damaged one, assuming that is the case, then there isn't a perfect repair process =/

P.S. Here's DNA damage theory of aging

Further searching I did finds that sperm comes from testes' germ cell, but stem cell still goes through DNA damage

Edited August 13, 2016 by fredreload

[jimmydasaint]

So as I've mentioned before. If the cell divide with mitosis, it would produce an identical cell at the same age. Just like I am age 30, so my cell would go through mitosis and produce an identical cell of age 30. Now here is my question about aging, when a cell goes through meiosis it produces cells with chromosomes that are halved known as gametes(sperm and egg). When sperm and egg combines, it produces a zygote which is of age zero (something that will turn into a baby). Now how does a human of age 30 produces sperm of age zero with meiosis? Some suggests that telomere is the key to aging, but when sperm is produced, is the telomere completely restored? I'm pretty sure normally there wouldn't be any defects to the babies, and humans doesn't give birth to a baby with shorter telomere, that means to reverse aging or to set the DNA back to its zero state is done in meiosis and all we have to do is to open a sperm and check its DNA to find out. If the sperm's DNA has a longer telomere, then we know it is restored in the meiosis process. If it is not, then something else might be at work.

Then there is the DNA damage theory, the DNA damage theory says that your DNA gets damaged as you grow older, but I think the zygote or babies can't possibly grow up with damaged DNA from the sperm, that means the DNA must also be repaired in the meiosis process. If the DNA is not repaired, then we know that DNA damage does not contribute to aging, all that matters is the telomere, or something else. I would like to know what you think Strange if you are reading this post

 

I don't understand why this is posted in the "speculations" thread. Nevertheless, the restoration of telomere length is a poorly understood process, but this seems to occur at an early developmental stage, not during meiosis but possibly during post-fertilisation mitosis, if I have read this paper correctly:

 

I gave you a fairly long quote without editing by me:

 

Stem cells and cancer cells maintain telomere length mostly through telomerase^{1, 2, 3}. Telomerase activity is high in male germ line and stem cells, but is low or absent in mature oocytes and cleavage stage embryos, and then high again in blastocysts³. How early embryos reset telomere length remains poorly understood. Here, we show that oocytes actually have shorter telomeres than somatic cells, but their telomeres lengthen remarkably during early cleavage development. Moreover, parthenogenetically activated oocytes also lengthen their telomeres, thus the capacity to elongate telomeres must reside within oocytes themselves. Notably, telomeres also elongate in the early cleavage embryos of telomerase-null mice, demonstrating that telomerase is unlikely to be responsible for the abrupt lengthening of telomeres in these cells.

 

 

http://www.nature.com/ncb/journal/v9/n12/full/ncb1664.html

[fredreload]

 

I don't understand why this is posted in the "speculations" thread. Nevertheless, the restoration of telomere length is a poorly understood process, but this seems to occur at an early developmental stage, not during meiosis but possibly during post-fertilisation mitosis, if I have read this paper correctly:

 

I gave you a fairly long quote without editing by me:

 

 

http://www.nature.com/ncb/journal/v9/n12/full/ncb1664.html

Well, our focus right now is on the DNA damage theory and having telomere being part of the DNA sequence we are just looking it as a whole. I'm bringing in the quote from Wikipedia

 

The DNA damage theory of aging proposes that aging is a consequence of unrepaired accumulation of naturally occurring DNA damages.

Now why is it that none of this DNA damages is passed down to the offspring when all the DNA in all the cells are getting damaged?

 

In estimates made for mice, on average approximately 1,500 to 7,000 DNA lesions occur per hour in each mouse cell, or about 36,000 to 160,000 per cell per day.

So I speculate that, well the germ cells contain an unbreakable copy of the DNA, ready to create sperm cells

 

 

Edited August 13, 2016 by fredreload

[jimmydasaint]

With respect, your OP is what I answered. That subject is not closed unless you comment on the paper extract that I gave you and then we come to a conclusion. If you are creating another question, why not start a new thread?

[fredreload]

With respect, your OP is what I answered. That subject is not closed unless you comment on the paper extract that I gave you and then we come to a conclusion. If you are creating another question, why not start a new thread?

Right well, I did mention DNA damage theory in the op. I just don't feel that there is a need to start a new thread consider most of the materials are already presented here. If you feel there is a need I can start a new one tomorrow

[Fuzzwood]

"Now why is it that none of this DNA damages is passed down to the offspring when all the DNA in all the cells are getting damaged?"

 

Aren't they? DNA damage doesn't automatically mean the ensuing enzyme or whatever the damaged part codes for is immediately non-functional. And if it is, well, miscarriages happen quite often.

 

Also don't forget that DNA is quite capable of repairing itself.

Edited August 13, 2016 by Fuzzwood

[fredreload]

"Now why is it that none of this DNA damages is passed down to the offspring when all the DNA in all the cells are getting damaged?"

 

Aren't they? DNA damage doesn't automatically mean the ensuing enzyme or whatever the damaged part codes for is immediately non-functional. And if it is, well, miscarriages happen quite often.

 

Also don't forget that DNA is quite capable of repairing itself.

If DNA is capable of perfect repair then you wouldn't age, the repair is not perfect

 

Edited August 14, 2016 by fredreload

[Endy0816]

I think you are thinking that cells are all damaged at the same rate, which is not the case. Basically random.

[fredreload]

I think you are thinking that cells are all damaged at the same rate, which is not the case. Basically random.

Really? That does not make much sense to me. That means parts of my body would age faster than other parts of my body. Where is this information from?

 

P.S. Hmm it seems you just proved that it's not possible = =

Edited August 15, 2016 by fredreload

[Endy0816]

http://www.nytimes.com/2005/08/02/science/your-body-is-younger-than-you-think.html?_r=0

[fredreload]

http://www.nytimes.com/2005/08/02/science/your-body-is-younger-than-you-think.html?_r=0

Right well, I agree that different tissue type might have a different division rate, but if we look the arm for example, my left arm does not age older then my right arm normally. It can be bigger, but they generally do grow at the same rate. And don't show me a picture of someone with two different aging arms I'm saying normal cases.

 

P.S. My speculation is, if similar cells age at the same rate, then they must be controlled, not damaged

P.S. Programmed theory of aging, I'm surprised we haven't found that gene

Edited August 15, 2016 by fredreload