Why cloned offsprings die earlier?

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Discussion Overview

The discussion revolves around the phenomenon of cloned offspring experiencing accelerated aging and shorter lifespans. Participants explore potential biological mechanisms, including genetic imprinting and telomere length, while considering the implications of cloning technology.

Discussion Character

  • Exploratory
  • Debate/contested
  • Technical explanation

Main Points Raised

  • One participant suggests that problems with cloning may relate to genetic imprinting and telomere length, speculating on the implications of these factors for cloned animals' health.
  • Another participant questions the relevance of telomere shortening to premature aging, recalling a past debate on the topic and emphasizing the uncertainty surrounding the mechanisms at play.
  • A different viewpoint highlights that a 'true' clone has not yet been achieved in higher organisms, pointing out the complexity of gene activation and the timing of gene expression during development.
  • One participant asserts that while imprinting is a concern, telomeres may not be a significant factor, reflecting ongoing discussions about the role of these biological elements in cloning.

Areas of Agreement / Disagreement

Participants express differing views on the significance of telomere shortening in relation to cloned offspring's aging, with some agreeing that imprinting is a problem while others contest the role of telomeres. The discussion remains unresolved regarding the exact causes of premature aging in cloned animals.

Contextual Notes

Participants acknowledge that the understanding of cloning technology and its implications is still developing, with many aspects remaining poorly understood.

Saint
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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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