Why cloned offsprings die earlier?

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Cloning raises significant concerns regarding the health and longevity of cloned offspring, particularly due to issues related to genetic imprinting and telomere length. Genetic imprinting affects the expression of genes that should be turned on or off in adult cells, which may lead to health deterioration in clones. Telomeres, which protect chromosome ends, shorten with each cell division. Cloned animals derived from adult cells start with already shortened telomeres, potentially leading to a reduced lifespan. While telomerase can rebuild telomeres, it may not sufficiently counteract the effects of initial shortening. The complexities of gene activation during development further complicate cloning, as a true clone has yet to be achieved in higher organisms. The mechanisms behind these phenomena remain poorly understood, highlighting the challenges and uncertainties in cloning technology.
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The cloned offsprings grow from baby, but later they become old faster and die earlier, why ? :frown:
 
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There's many problems with cloning, and I think one of the main problems is to do with imprinting and telomere length. (I'm kind of speculating, because I only skim through the topic when evaluating it for a uni essay, but chose telomerase instead)

Imprinting is where some genes that are normally on (or off) in an adult cell are turned off in gamete cells - which doesn't normally occur with cloned cells. For example, if an adult forms of a protein are produced when a cloned animal is young, it could lead to deteriorated health.

And telomeres are repeats of a nucleotide that capt the ends of all chromosomes, and it prevents chromosomal instabilities. Each time a cell divides, these repeats get shorter. Normally, in gametes, telomerase (a protein) rebuilds the ends of a chromosome. But a nucleus extracted from an adult cell would already have shortened telomeres - possibly reducing life span. I'm sure researchers have found a way around this.. but who knows, perhaps artifically induced telomerase doesn't add enough length.

Hmm.. hopefully all this points you in the right direction... which may be wrong.
 
I can't recall if the phenomenon of telomere shortening is still considered to be a part of it or not. I seem to recall a debate about that a while back, that it might not account for the premature aging.

I think the bottom line is we don't really know what goes wrong. This is fairly new technology, and a lot of things aren't well understood yet.
 
Agree with Jikx. A 'true' clone has not been made, at least in higher organisms. The genetic sequence includes a number of active and inactive genes. Not only must the all the genes be in the correct on-off position when cell division is initiated, they must be switched to the correct on-off position at the right time during both embryonic and post-embryonic development. How this 'programming' works is not understood.
 
Imprinting is a problem, telomeres don't seem to be (last I heard).
 
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