Home About us Contact
|
Home About us Contact | ||
|
|
||
Fitness Loss (fitness + loss)
Selected AbstractsAmbient ultraviolet-B radiation reduces hatchling size in the common frog Rana temporariaECOGRAPHY, Issue 5 2000Maarit Pahkala Effects of ambient UV-B radiation and pH on hatchability and early development of Rana temporaria embryos were studied in field experiments conducted at two sites in Sweden. In neither of the populations did we find clear evidence for reduced hatchability or increased frequency of developmental anomalies of embryos exposed to ambient UV-B levels. However, in both populations hatchling size was significantly larger UV-B blocked as compared to control treatments, suggesting that ambient UV-B levels had a negative effect on early growth of embryos. This result is consistent with the hypothesis that the cellular UV-B damage repair mechanisms are costly and trades-off against early growth. Alternatively, UV-B induced photoproducts inhibiting DNA-transcription and thereby protein synthesis may directly reduce growth rate. Although low pH (5.0) had negative effects on hatchability and early embryonic growth, there was no evidence for synergistic effects of pH and UV-B on hatchability, frequency of developmental anomalies or early growth. The results suggest that increased levels of UV-B radiation may cause fitness loss in natural populations of the common frog. [source] INTERPOPULATION HYBRID BREAKDOWN MAPS TO THE MITOCHONDRIAL GENOMEEVOLUTION, Issue 3 2008Christopher K. Ellison Hybrid breakdown, or outbreeding depression, is the loss of fitness observed in crosses between genetically divergent populations. The role of maternally inherited mitochondrial genomes in hybrid breakdown has not been widely examined. Using laboratory crosses of the marine copepod Tigriopus californicus, we report that the low fitness of F3 hybrids is completely restored in the offspring of maternal backcrosses, where parental mitochondrial and nuclear genomic combinations are reassembled. Paternal backcrosses, which result in mismatched mitochondrial and nuclear genomes, fail to restore hybrid fitness. These results suggest that fitness loss in T. californicus hybrids is completely attributable to nuclear,mitochondrial genomic interactions. Analyses of ATP synthetic capacity in isolated mitochondria from hybrid and backcross animals found that reduced ATP synthesis in hybrids was also largely restored in backcrosses, again with maternal backcrosses outperforming paternal backcrosses. The strong fitness consequences of nuclear,mitochondrial interactions have important, and often overlooked, implications for evolutionary and conservation biology. [source] Evolution of mutation rates in bacteriaMOLECULAR MICROBIOLOGY, Issue 4 2006Erick Denamur Summary Evolutionary success of bacteria relies on the constant fine-tuning of their mutation rates, which optimizes their adaptability to constantly changing environmental conditions. When adaptation is limited by the mutation supply rate, under some conditions, natural selection favours increased mutation rates by acting on allelic variation of the genetic systems that control fidelity of DNA replication and repair. Mutator alleles are carried to high frequency through hitchhiking with the adaptive mutations they generate. However, when fitness gain no longer counterbalances the fitness loss due to continuous generation of deleterious mutations, natural selection favours reduction of mutation rates. Selection and counter-selection of high mutation rates depends on many factors: the number of mutations required for adaptation, the strength of mutator alleles, bacterial population size, competition with other strains, migration, and spatial and temporal environmental heterogeneity. Such modulations of mutation rates may also play a role in the evolution of antibiotic resistance. [source] COMPENSATING FOR OUR LOAD OF MUTATIONS: FREEZING THE MELTDOWN OF SMALL POPULATIONSEVOLUTION, Issue 5 2000Art Poon Abstract We have investigated the reduction of fitness caused by the fixation of new deleterious mutations in small populations within the framework of Fisher's geometrical model of adaptation. In Fisher's model, a population evolves in an n -dimensional character space with an adaptive optimum at the origin. The model allows us to investigate compensatory mutations, which restore fitness losses incurred by other mutations, in a context-dependent manner. We have conducted a moment analysis of the model, supplemented by the numerical results of computer simulations. The mean reduction of fitness (i.e., expected load) scaled to one is approximately n/(n + 2Ne), where Ne is the effective population size. The reciprocal relationship between the load and Ne implies that the fixation of deleterious mutations is unlikely to cause extinction when there is a broad scope for compensatory mutations, except in very small populations. Furthermore, the dependence of load on n implies that pleiotropy plays a large role in determining the extinction risk of small populations. Differences and similarities between our results and those of a previous study on the effects of Ne and n are explored. That the predictions of this model are qualitatively different from studies ignoring compensatory mutations implies that we must be cautious in predicting the evolutionary fate of small populations and that additional data on the nature of mutations is of critical importance. [source] | ||||||||||