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Deinococcus radiodurans is an amazing bacterium with a fantastic survival rate. It can survive to high doses of radiation, in a complete vacuum and in hydrochloric acid.

How does this bacterium manage to restore damaged chromosome? It is polyploid with 4 to 10 copies of the genome which are packed in a highly ordered manner.

Does this imply that creating multiple copies of the genome or inceasing DNA base repair activity would increase life span? Is that even conceivable on bigger life forms?

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Could you please try to clarify your question, I have a hard time understanding what exactly you are trying to ask. –  Mad Scientist Nov 17 '12 at 13:36
    
I have tried to edit your question. I still can't understand what you are asking. Do you believe that simply increasing ploidity will boost life span? –  terdon Nov 17 '12 at 16:59
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Upon reading the article: yes seems rigid packaging, no less important than the number of copies of the genome. Over time, the chromosomes are scattered and pile –  Aaron Livni Nov 17 '12 at 21:22

1 Answer 1

It's an idea that doesn't hold much promise.

Individuals who show diploid/tetraploid mosaicism present "failure to thrive and multiple minor anomalies." according to:

Alonso L et al (2002) Tetraploid/diploid mosaicism: case report and review of the literature. Annales de Genetique 45 177-180

On the other hand, complete tetraploidy is apparently lethal:

Nakamura, Y. et al. (2003) A Tetraploid Liveborn Neonate: Cytogenetic and Autopsy Findings. Archives of Pathology & Laboratory Medicine 127:1612-1614.

Abstract

Cytogenetic and autopsy findings of a nonmosaic tetraploid male neonate, alive until shortly after birth at 37 weeks' gestation, are described. Oligohydramnios, intrauterine growth retardation, cranial abnormalities, and Dandy-Walker malformation were noted prenatally. Autopsy findings included cleft lip and palate; overlapping fingers; low-set ears; simian creases; hypoplastic external genitalia with undescended testes; Dandy-Walker malformation; slightly dilated lateral and third ventricles; hypoplasia of the cerebrum, pons, medulla, pituitary gland, thymus, lung, adrenal gland, and kidney; large ventricular septal defect; and enteric cyst behind the urinary bladder. The placenta was hypoplastic and showed no remarkable abnormalities, except for mild syncytial knots. Chromosome analyses of amniotic fluid cells at 31 weeks' gestation and the umbilical cord blood cells at delivery revealed a 92,XXYY karyotype. G-, C-, Q-, and N-banding heteromorphic studies demonstrated duplication of paternal chromosomes 1, 3, and 15, and maternal chromosome 22. In addition, the results of an analysis with 16 CA repeat polymorphic markers were consistent with duplicated inheritance of 1 paternal and 1 maternal haploid sets to the tetraploid patient. Therefore, it is most likely that the tetraploidy was caused by a cytoplasmic cleavage failure at the first mitotic division.

full text available here.

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