Abstract: About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention.

Abstract: Psychologists, economists, and advertising moguls have long known that human decision-making is strongly influenced by the behavior of others. A rapidly accumulating body of evidence suggests that the same is true in animals. Individuals can use information arising from cues inadvertently produced by the behavior of other individuals with similar requirements. Many of these cues provide public information about the quality of alternatives. The use of public information is taxonomically widespread and can enhance fitness. Public information can lead to cultural evolution, which we suggest may then affect biological evolution.

Abstract: We have identified and extensively characterized a type IV collagen alpha chain, referred to as alpha 5(IV). Four overlapping cDNA clones isolated contain an open reading frame for 543 amino acid residues of the carboxyl-terminal end of a collagenous domain, a 229-residue carboxyl-terminal noncollagenous domain, and 1201 base pairs coding for a 3' untranslated region. The collagenous Gly-Xaa-Yaa repeat sequence has five imperfections that coincide with those in the corresponding region of the alpha 1(IV) chain. The noncollagenous domain has 12 conserved cysteine residues and 83% and 63% sequence identity with the noncollagenous domains of the alpha 1(IV) and alpha 2(IV) chains, respectively. The alpha 5(IV) chain has less sequence identity with the putative bovine alpha 3(IV) and alpha 4(IV) chains. Antiserum against an alpha 5(IV) synthetic peptide stained a polypeptide chain of about 185 kDa by immunoblot analysis and immunolocalization of the chain in human kidney was almost completely restricted to the glomerulus. The gene was assigned to the Xq22 locus by somatic cell hybrids and in situ hybridization. This may be identical or close to the locus of the X chromosome-linked Alport syndrome that is believed to be a type IV collagen disease.

Abstract: The colours of the horses have long been a subject of interest to owners and breeders of horses as well as to scientists. Though, the colour of horses has little to do with its performance, it is a primary means of identification and also the first indicator of questionable parentage. Probably the ancestral colour of the horse was a black-based pattern that provided camouflage protection against predators. Horse colours are mostly controlled by genes at 12 different loci. The three basic colours of horses are black, bay and chestnut. The genetic control of the basic colours of horses resides at two genetic loci, namely Extension (E) and Agouti (A) loci. Among the basic colours bay is dominant to black and both are epistatic to chestnut. Dilution of basic colours of horses as a result of four colour dilution genes such as cream dilution, dun, silver dapple and champagne resulted in extensive array of possible colours of horses. The most widespread and familiar of the horse colour dilution gene is the one that produces the golden body colour and are called as palomino or buckskin based on the colour of the points. The grey coat colour is due to the presence of dominant gene (G) at the grey locus. Grey is epistatic to all coat colour genes except white and a grey horse must have at least one grey parent. Roan is due to a dominant gene (Rn) at roan locus and this combines with any base colour to produce the various shades of roan pattern. White coat is due to a single dominant gene (W) and it is epistatic to the genes controlling all other colours. White marking in the face and legs are due to genetic and non-genetic factors. Several genes are involved in producing white markings. During recent years, comparative genomics and whole genome scanning have been used to develop DNA tests for different variety of horse colours. Molecular genetic studies on coat colour in horses helped in identification of the genes and mutation responsible for coat colour variants. In future, this will be applied to breeding programmes to reduce the incidence of diseases and to increase the efficiency of race horse population.

Abstract: The host preference, survival rates, and length of the gonotrophic cycle of Anopheles punctimacula was investigated in southern Mexico. Mosquitoes were collected in 15-day separate experiments during the rainy and dry seasons. Daily changes in the parous-nulliparous ratio were recorded and the gonotrophic cycle length was estimated by a time series analysis. Anopheles punctimacula was most abundant during the dry season and preferred animals to humans. The daily survival rate in mosquitoes collected in animal traps was 0.96 (parity rate = 0.86; gonotrophic cycle = 4 days). The length of gonotrophic cycle of 4 days was estimated on the base of a high correlation coefficient value appearing every 4 days. The minimum time estimated for developing mature eggs after blood feeding was 72 h. The proportion of mosquitoes living enough to transmit Plasmodium vivax malaria during the dry season was 0.35.