Hughes et al. (2002) found experimental evidence that inbreeding depression incr
ID: 82748 • Letter: H
Question
Hughes et al. (2002) found experimental evidence that inbreeding depression increased with age in a population of Drosophila. Their work implies:
The expression of deleterious mutations increases with age.
Extrinsic mortality is irrelevant.
New mutations are steadily occurring within each individual's somatic cells as they age, causing senescence in proportion to age.
Natural selection has been less effective at removing deleterious mutations in proportion to the age at which they are expressed
Selection for long lifespan has exhausted genetic variation for that trait.
The expression of deleterious mutations increases with age.
Extrinsic mortality is irrelevant.
New mutations are steadily occurring within each individual's somatic cells as they age, causing senescence in proportion to age.
Natural selection has been less effective at removing deleterious mutations in proportion to the age at which they are expressed
Selection for long lifespan has exhausted genetic variation for that trait.
a.The expression of deleterious mutations increases with age.
b.Extrinsic mortality is irrelevant.
c.New mutations are steadily occurring within each individual's somatic cells as they age, causing senescence in proportion to age.
d.Natural selection has been less effective at removing deleterious mutations in proportion to the age at which they are expressed
e.Selection for long lifespan has exhausted genetic variation for that trait.
Explanation / Answer
a) Evolutionary theories of aging state that the accumulation of deleterious mutations will reduce life span. Researcher's have observed in Drosophila melanogaster. Experiment design is a newly designed mating scheme, in which mutations acquired an increasing number on the Binscy balancer X chromosome in heterozygous females in the absence of selection and recombination and reported that the life span of Binscy/RYL males from this cross decreased faster as compared with the life span of their sibling controls over time in two of three runs. Above all they suggested that there was an age-specific increase in mortality in the Binscy/RYL males with time in one of three runs. Thus, suggested that the acquire of increasing number of deleterious mutations can decrease life span by increasing fragility and can cause age-specific changes in mortality.
b) The evolutionary theories of aging reflects complex mechanisms underlying senescence. Classical theories state that high levels of extrinsic mortality should acquired from the evolution among shorter lifespans and earlier peak fertility. However, Non-classical theories state, that an increase in extrinsic mortality may acquired among the evolution of longer lifespans. With the help of a stochastic, agent-based, computational mode it was reported by researcher's that longer or shorter lifespans was adapted because of increased or decreased in investments of energy into somatic maintenance. Thus suggesting that higher predation causes significantly decreased in total population size by enlarging the shared resource pool and result in difficulty to acquire energy reserves for mature individuals.
(c) Aging provides important reasons to understand the cause of age-related physiological changes. A recent method has been developed which does not require cell division for the direct measurement of genetic variants in mammalian cells in culture and is therefore suitable for ageing studies. Literature suggests that these variants are mutations. It was reported that the frequency increased gradually during the lifespan of the culture and regression analysis shows that the increase in growth is dependent on factors. Moreover, variant frequency can not be immortal transformed for over 100 passages. This attributed that the variants are regulatory mutations. This is indicative of the involvement of presumed somatic mutations in the ageing of mammalian cells. Thus, suggested new mutations are steadily occurring within each individual's somatic cells as they age, causing senescence in proportion to age.
(d) The degree to which natural selection removes deleterious mutations from a population depend on factors like the selection coefficient (s) of a mutation and the population size (N). The hypotheisi was tested on the basis of per-genome accumulation of non-synonymous substitutions across diverse pairs of populations. It signify a higher load of deleterious mutations in non-Africans. However, significant differences among more divergent populations lead to an archaic Denisovans that resut in non-synonymous mutations which is faster than either modern humans or Neanderthals. To find consistency with patterns observed that removal of deleterious mutations in non-Africans is less efective than in West Africans. Thus suggested that the observed patterns are not likely to reflect changes in the effectiveness of selection after the populations split rather are more likely to be driven by other population genetic factors.
(e) Many Drosophila melanogaster populations continually end up at young adult ages but keep possession of surprisingly long postselection lifespans. It was reported from the Ives population by demonstrating that postselective longevity was both substantial (30 days) and temporally stable over time. Moreover, alleles with positive pleiotropic effects between adjacent ages, particularly those affecting overall condition, have been integrated into the theory and is responsible for the extended longevity observed. The hypothesis was tested by isolating 20 hemiclones from Ives and allowing spontaneous mutations to accumulate (MA) for 35 generations. control females is positively genetically correlated which is indicative of Fitness and longevity and both traits declined due to MA. With decisive MA induced a strong positive genetic correlation between the traits in both sexes, attributed that mutations with early-life impacts also reduce late-life survival.Thus,suggested that extended postreproductive longevity is actively maintained not merely a byproduct of exhaustion of genetic variation or weak drift selection rather for early-life fitness via positive pleiotropy. Thus, mutation-selection balance for early fitness may govern variance in longevity in this system suggesting a selection for long lifespan has exhausted genetic variation for that trait.
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