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1.
Genet. mol. res. (Online) ; 5(4): 632-637, 2006. ilus
Article in English | LILACS | ID: lil-482092

ABSTRACT

Drosophila mulleri (MU) and D. arizonae (AR) are cryptic species of the mulleri complex, mulleri subgroup, repleta group. Earlier cytogenetic studies revealed that these species have different regulatory mechanisms of nucleolar organizing activity. In these species, nucleolar organizing regions are found in both the X chromosome and the microchromosome. In the salivary glands of hybrids between MU females and AR males, there is an interspecific dominance of the regulatory system of the D. arizonae nucleolar organizer involving, in males, amplification and activation of the nucleolar organizer from the microchromosome. The authors who reported these findings obtained hybrids only in that cross-direction. More recently, hybrids in the opposite direction, i.e., between MU males and AR females, have been obtained. The purpose of the present study was to evaluate, in these hybrids, the association of the nucleoli with the chromosomes inherited from parental species in order to cytogenetically confirm the dominance patterns previously described. Our results support the proposed dominance of the AR nucleolar organizer activity over that of MU, regardless of cross-direction.


Subject(s)
Animals , Female , Male , X Chromosome/genetics , Drosophila/genetics , Hybridization, Genetic/genetics , Cell Nucleolus/genetics , Nucleolus Organizer Region/genetics , Crosses, Genetic , Genetic Variation , Inheritance Patterns/genetics
2.
Indian J Hum Genet ; 1997 Apr; 3(2): 71-76
Article in English | IMSEAR | ID: sea-159808

ABSTRACT

(RSAs) revealed the presence of a supernumerary, metacentric, bisatellited microchromosome marker in the male partner. His karyotype was 47,XY,+mar. Molecular analysis revealed the marker to be an idic 14 or 22 (q11-12). We herein discuss two aspects with respect to the presence of the marker: firstly, the karyotype-phenotype relationship in the carrier as well as the possibility of the marker causing abnormality in the next generation and, secondly, the possible role of the marker in the causation of RSAs.

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