RESUMO
Genomewide scan, as shown by recently published linkage studies on the behavior of mice or in psychiatry, provides evidence for replicated quantitative trait loci (QTL). Several studies of Alzheimer's disease have demonstrated the promise of moving from clinical diagnoses to biological signs for psychiatric investigations. Empirical studies also demonstrate that genetic background, differences in environment, epistatic effects, and definition of the phenotype (including psychiatric diagnosis) all actively contribute to limit the duplication of QTL.
Assuntos
Mapeamento Cromossômico , Característica Quantitativa Herdável , Animais , Intervalos de Confiança , Ligação Genética , Genótipo , Humanos , Transtornos Mentais/genética , Camundongos , Modelos Genéticos , FenótipoRESUMO
The cerebellum is involved in a large set of integrative functions including memory, affect, and motricity. The cerebellar patterns of foliation and their causal relationships with motricity were investigated via a wide genome scan approach and quantitative trait locus (QTL) strategy. QTLs were mapped in an F2 population derived from NZB/B1NJ and C57BL/6By inbred strains of mice for cerebellar fissures in the four vermal lobules (intraculminate, uvula, declival, and intracentral) and for hindpaw slips in a bar crossing test. No linkage was detected for uvula and intracentral fissures. We found five QTLs linked to declival fissure: Cpfd-1q and Cpfd-2q (chromosome 1), Cpfd-3q (chromosome 5), Cpfd-4q (chromosome 9), and Cpfd-5q (chromosome 13). Two QTLs were also mapped for intraculminate fissure Cpfi-1q (chromosome 4) and Cpfi-2q (chromosome 1). Most of the confidence intervals of these QTLs included genes that were previously identified for their implication in the physiological mechanisms underlying cerebellar patterns of foliation. Only one significant QTL was found for the measure of hindpaw coordination (Tne-1q). It was linked with Cpfd-1q and Cpfd-2q on the telomeric part of chromosome 1.
