			Home About us Contact

Many Phenotypes (many + phenotype)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

A new genetic algorithm with diploid chromosomes using probability decoding for adaptation to various environments

ELECTRONICS & COMMUNICATIONS IN JAPAN, Issue 8 2010
Manabu Kominami
Abstract This paper proposes a new diploid operation technique using probability for function optimization in nonstationary environments and describes a feature of diploid genetic algorithms (GAs). The advantage of the technique over previous diploid GAs is that one genotype is transformed into many phenotypes based on probability. This transformation is not made at random. It has a certain range of probabilities. Each individual has a range. The range allows adaptation to various environments. The technique allows genes to give a probabilistic representation of dominance, and can maintain the diversity of individuals. The experimental results show that the technique can adapt to severe environmental changes where previous diploid GAs cannot adapt. This paper shows that the technique can find optimum solutions with high probability and that the distribution of individuals changes when the environment changes. In addition, by comparing the proposed diploid GA with a haploid GA whose chromosome is twice the length, the features of the diploid are described. © 2010 Wiley Periodicals, Inc. Electron Comm Jpn, 93(8): 38,46, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecj.10097 [source]

Deficits in acetylcholine homeostasis, receptors and behaviors in choline transporter heterozygous mice

GENES, BRAIN AND BEHAVIOR, Issue 5 2007
M. H. Bazalakova
Cholinergic neurons elaborate a hemicholinium-3 (HC-3) sensitive choline transporter (CHT) that mediates presynaptic, high-affinity choline uptake (HACU) in support of acetylcholine (ACh) synthesis and release. Homozygous deletion of CHT (,/,) is lethal shortly after birth (Ferguson et al. 2004), consistent with CHT as an essential component of cholinergic signaling, but precluding functional analyses of CHT contributions in adult animals. In contrast, CHT+/, mice are viable, fertile and display normal levels of synaptosomal HACU, yet demonstrate reduced CHT protein and increased sensitivity to HC-3, suggestive of underlying cholinergic hypofunction. We find that CHT+/, mice are equivalent to CHT+/+ siblings on measures of motor co-ordination (rotarod), general activity (open field), anxiety (elevated plus maze, light/dark paradigms) and spatial learning and memory (Morris water maze). However, CHT+/, mice display impaired performance as a result of physical challenge in the treadmill paradigm, as well as reduced sensitivity to challenge with the muscarinic receptor antagonist scopolamine in the open field paradigm. These behavioral alterations are accompanied by significantly reduced brain ACh levels, elevated choline levels and brain region-specific decreased expression of M1 and M2 muscarinic acetylcholine receptors. Our studies suggest that CHT hemizygosity results in adequate baseline ACh stores, sufficient to sustain many phenotypes, but normal sensitivities to physical and/or pharmacological challenge require full cholinergic signaling capacity. [source]

Two modes of mitochondrial dysfunction lead independently to lifespan extension in Caenorhabditis elegans

AGING CELL, Issue 3 2010
Wen Yang
Summary In Caenorhabditis elegans, longevity is increased by a partial loss-of-function mutation in the mitochondrial complex III subunit gene isp-1. Longevity is also increased by RNAi against the expression of a variety of mitochondrial respiratory chain genes, including isp-1, but it is unknown whether the isp-1(qm150) mutation and the RNAi treatments trigger the same underlying mechanisms of longevity. We have identified nuo-6(qm200), a mutation in a conserved subunit of mitochondrial complex I (NUDFB4). The mutation reduces the function of complex I and, like isp-1(qm150), results in low oxygen consumption, slow growth, slow behavior, and increased lifespan. We have compared the phenotypes of nuo-6(qm200) to those of nuo-6(RNAi) and found them to be distinct in crucial ways, including patterns of growth and fertility, behavioral rates, oxygen consumption, ATP levels, autophagy, and resistance to paraquat, as well as expression of superoxide dismutases, mitochondrial heat-shock proteins, and other gene expression markers. RNAi treatments appear to generate a stress and autophagy response, while the genomic mutation alters electron transport and reactive oxygen species metabolism. For many phenotypes, we also compared isp-1(qm150) to isp-1(RNAi) and found the same pattern of differences. Most importantly, we found that, while the lifespan of nuo-6, isp-1 double mutants is not greater than that of the single mutants, the lifespan increase induced by nuo-6(RNAi) is fully additive to that induced by isp-1(qm150), and the increase induced by isp-1(RNAi) is fully additive to that induced by nuo-6(qm200). Our results demonstrate that distinct and separable aspects of mitochondrial biology affect lifespan independently. [source]

Animal models of Williams syndrome,

AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 2 2010
Lucy R. Osborne
Abstract In recent years, researchers have generated a variety of mouse models in an attempt to dissect the contribution of individual genes to the complex phenotype associated with Williams syndrome (WS). The mouse genome is easily manipulated to produce animals that are copies of humans with genetic conditions, be it with null mutations, hypomorphic mutations, point mutations, or even large deletions encompassing many genes. The existing mouse models certainly seem to implicate hemizygosity for ELN, BAZ1B, CLIP2, and GTF2IRD1 in WS, and new mice with large deletions of the WS region are helping us to understand both the additive and potential combinatorial effects of hemizygosity for specific genes. However, not all genes that are haploinsufficient in humans prove to be so in mice and the effect of genetic background can also have a significant effect on the penetrance of many phenotypes. Thus although mouse models are powerful tools, the information garnered from their study must be carefully interpreted. Nevertheless, mouse models look set to provide a wealth of information about the neuroanatomy, neurophysiology and molecular pathways that underlie WS and in the future will act as essential tools for the development and testing of therapeutics. © 2010 Wiley-Liss, Inc. [source]