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17

I disagree with Ctina. So many factors go into determining loss rate, activity of telomerase, gene conversion or unequal exchange at chromosome ends, etc to ever say that length is a function of age. There is far more variation between individuals and between cells within an individual than aging ever shows. Here is one study: Das B, Saini D, Seshadri M. ...


15

I've been doing some reading, and have come up with the following interesting information. Telomeres During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess ...


11

Hydra are just one of the many organisms which are immortal. That is to say all their cells divide forever - there is no senescence (planned cell death) in any of their cells. Interestingly Hydrae that reproduce sexually age and die, but asexual reproduction appear to be immortal. Animals that are immortal more often reproduce asexually... this may only ...


10

Gametes (sperm and ovum), which fuse to form a zygote, arise from germ cells (spermatogonia and oogonia). Germ cells, like stem cells, are maintained carefully i.e the genome is preserved and transposition/recombination events are tightly controlled via different mechanisms. So these germ cells don't have shortened telomeres. Also, during early embryonic ...


8

It would be reliable if we don't take into account the environment, and if we are comparing two genetically identical persons. First, because there are many other factors that can cause genetic mutation and consequently shorten lifespan. Second, giving an extreme example and not taking into account the environment and modern medicine, we cannot expect a ...


7

Interesting question. My answer is no, but it requires a rather science-fiction style answer - at least it's beyond current technology, but here goes: My Assumptions I make the simplifying assumption that ageing is only related to telomere length. Thus by "avoid ageing" I assume you mean "avoid telomere shortening". Also to clarify things for others, I'll ...


7

Again, not an expert, but I found this article seems to say it pretty well: Telomere's are most commonly measured by qPCR of the repetitive regions with degenerate oligomer sequences such as "TTAGGG and CCCTAA repeats" Although articles like this one appear to advance measurements in vertebrates, this reference from 2011 implies two techniques continue to ...


5

Nope, nope, and nope. A cursory glance over any page on hematopoesis will reveal that blood cells are replenished from HSC, hematopoetic stem cells, which are self-renewing stem cells. Telomerase is activated in stem cells.


4

Telomeres do not "cause" ageing as such - although you are right that they limit the number of times a somatic cell can divide. Each time a cell divides the chromosomes are replicated in an imperfect way, and as such a small amount of DNA is lost from the end of the chromosome during each round of cell division. Telomeres are just extensions to the ...


4

In a normal cell, during each replication the telomere is shortened slightly due to the end replication problem, as you probably know. As mutations occur and a normal cell begins to exhibit cancerous characteristics, it needs a way to stop the self-destruction which happens when the telomeres become too short. In fact it is the cancer cells themselves which ...


3

Telomerases are tightly controlled on all level: Expression, post-translational modifications and by external factors. I think for this the external factors, a protein class called telomeric proteins. They bind to the end of the telomere and regulate the telomerase. The figure is from this paper, which looks into the topic quite extensively: Regulation ...


3

A database that answers the question, charting telomere repeat sequences for all known species, is: http://telomerase.asu.edu/sequences_telomere.html For example in Yeast:


3

In replication, both the chromosomal halves (which are simultaneously threaded through the replication complex) have a lagging and a leading strand. A part of the segment will be replicated as leading and a part as lagging.


3

A number of studies have compared replicative capacity of cells with lifespan. Since Replicative capacity of cells is linked to telomere-length, these studies may provide indirect evidence for the association between telomere length and lifespan. One interesting study in particular compared animal life spans and in vitro replicative capacity of skin ...


3

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication. Telomeres are extensions to the end of ...


2

I have found that biogps.org has all expression data I need: https://biogps.org https://biogps.org/#goto=genereport&id=7015


2

It is not consistent, and so cannot function as a temporal or generational signal. Not because the telomere shortening is unpredictable, but because of telomerase activity in the embryo. If it did, gamete production in specialized tissues like the ovaries or testes would have shorter telomeres than the zygote they originated from. Each generation would have ...


2

It would be simpler to simply activate telomerase genes or insert them using some vector virus. However, telomerase is a key component in the process of tumoral transformation. Basically, if you don't let cells die they will stack mutations until they become tumoral.


2

Telomerase activity is just one (probably minor) facet of aging. It takes a lot more than just basic end repair of DNA to keep a complex organism alive, especially mammals. Just a few issues off the top of my head: repairing oxidative stress to DNA and proteins repairing UV damage to DNA keeping cells clean of debris like protein aggregate buildup (think ...


2

Actually, most adult cells do not express telomerase or express it only at a very low levels. Telmoerase is highly expressed only in cells that need to divide (e.g. stem cells), thus "immortalizing" them. In fact, human cell lines which scientists work with can be "immortalized" by activation of telomerase (along with other things). So you may ask yourself: ...


2

TTAGG telomeric repeats have been found in several insects. From Sahara, Marek & Traut (1): (TTAGG)n-containing telomeres were found in three Lepidoptera species, the silkworm Bombyx mori (in which the telomeric sequence was recently discovered), the flour moth Ephestia kuehniella, and the wax moth Galleria mellonella, in one species of ...


2

It seems that the current model is that recombination is the mechanism by which telomere length is maintained in the malaria vector Anopheles gambiae. Here is an exerpt of Roth et al paper that proposed the recombination mechanism: The insertion of a transgenic pUChsneo plasmid at the left end of chromosome 2 provided a unique marker for measuring the ...


2

Short answer: No. Eukaryotes have more ways of maintaining telomere length than via telomerase alone and all organisms with circular genomes do not need to worry about telomere length anyway. Long answer: Firstly, the telomerase system is not the only observed mechanism in Eukaryotes that elongates telomeres. Other mechanisms such as the transposition of ...


2

Here is a study of planarian worms, which are immortal in asexual reproduction and mortal in sexual reproduction. Hydras also become mortal after they reproduce sexually. Relevant to your question: Cells within planarian worm differ in expression of telomerase active subunit depending on body part. Immortal (asexual) worms have more expression in the area ...


2

A second telomerase is not necessary, as the lagging strand is filled in by the DNA-Polymerase, see this figure:


1

In cancer cells, the telomerase is not "formed" but activated, mainly due to an amplification and a gain of copy of the 5p chromosome arm, containing the gene coding for TERT. For example, a very common way to immortalize primary cells to establish a cell line is to stably express TERT. Shortened telomeres initiates DNA damage response pathways, resulting ...


1

This seems a bit like a hen and egg problem. Telomere length is both associated with age and with heart diseases, but heart disease is also associated with age. The question here is, is one really causing the other here (short telomeres heart problems) or do they occur simultaneously? The other problem with heart disease is that it is a multi-risk disease, ...


1

This is speculation, as I haven't done or read of the required experiment. However, I imagine that this would not be a problem. You're right that the RNA template (TERC) would not hybridize with a poly-G sequence, and so the telomerase would not be able to add more telomere repeats. You can imagine that the poly-G sequence is a cap, preventing telomerase ...


1

Many studies, including those of Hayflick himself, have found a strong correlation between a species' Hayflick limit and its maximum lifespan. For example, Galapagos tortoises, which can live over a century, have a Hayflick limit of 90-125, and mice, which live only a few years, have a Hayflick limit of 14-28. However, the mechanism connecting the maximum ...


1

After cloning, the recipient cell is converted into embryonic stem cell. When it is a stem cell, it can produce enzyme telomerase itself which a naturally occurring enzyme that maintains telomeres and prevents them from shortening during cell division in cells. So i think there are no problem on shortening of telomeres.



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