No description available.

No description available.

No description available.

The Drosophila melanogaster gene vasa is known to be necessary for the establishment of a functional pole plasm, as well as for the completion of oogenesis. To further elucidate its role, we have created a null mutation of the vasa gene and examined vasa-null ovaries for defects. Analysis of these ovaries has revealed that vasa is involved in various aspects of oogenesis, including the growth of germ-line cysts, oocyte differentiation, anterior-posterior egg chamber patterning, and dorsal-ventral follicle patterning. In addition, vasa-null oocytes fail to show efficient accumulation of various localized RNAs, such as Bicaudal-C, Bicaudal-D, egl, enc, orb, oskar , and nanos, but still show accumulation of gurken RNA. Interestingly, the accumulation of GURKEN protein in the oocyte is severely reduced, and that of BICAUDAL-C is substantially decreased in null mutants. These results suggest a possible role for vasa in activating translation of targeted RNAs during oogenesis.

Pole plasm in Drosophila melanogaster, through the posteriorly localized determinant nanos, controls the formation of the abdominal segments and, through an unknown mechanism, controls the formation of the germline. oskor, vasa, and tudor are three critical genes in the pole plasm assembly pathway and their gene products, oskar RNA, Vasa protein and Tudor protein are localized in the pole plasm in a precise order. The localization of oskar and nanos mRNAs is closely related to their translational activation. We provide evidence here by in vitro biochemical assays that Vasa protein is an ATP-dependent RNA helicase, an ATPase and an RNA-binding protein, as was predicted from its sequence similarity to mammalian translation initiation factor eIF-4A. The enzymatic activities of Vasa protein are important for its function, but the initial localization of Vasa protein to the pole plasm is independent of its RNA helicase and RNA-binding activities. Further, we cloned Bruno, a Xenopus etr-1 homologue with three ribonucleoprotein-recognition-motifs (RRM), by far-western screening using Vasa protein as bait. Bruno is the product of the gene arrest, which was cloned independently by Webster and Macdonald at Stanford University. The localization of Bruno protein in S1-10 oocytes is similar to that of oskar and gurken RNAs. This is significant as both oskar and gurken RNAs contain Bruno-response-elements at their 3$ sp prime$UTRs. Bruno is mislocalized in vasa mutant ovaries, suggesting that the localization of Bruno protein requires Vasa function. As a translational activator of oskar and nanos RNAs and a regulator of Bruno protein. the participation and the importance of Vasa protein in pole plasm assembly and function is obvious. Whether Vasa acts directly or indirectly to activate translation of specific mRNAs will require further examination.

Thesis (M.S.)--University of Hawaii at Manoa, 2007. / Includes bibliographical references (leaves 63-69). / 69 leaves, bound ill. (some col.) 29 cm

Bibliography: p. 133-141. / xviii, 154 p., [26] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / A genetic and molecular characterisation of the Drosophila gene starvin', focussing on analysis of the sequence of starvin', characterisation of the embryonic localisation of starvin' protein, and the identification and phenotypic characterisation of starvin' mutants. / Thesis (Ph.D.)--University of Adelaide, Dept. of Genetics, 2000

Thesis (Ph. D.)--University of Wisconsin--Madison, 1958. / Typescript. Abstracted in Dissertation abstracts, v. 18 (1958) no. 3, p. 1163. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 97-101).

Bibliography: p. 133-141. A genetic and molecular characterisation of the Drosophila gene starvin', focussing on analysis of the sequence of starvin', characterisation of the embryonic localisation of starvin' protein, and the identification and phenotypic characterisation of starvin' mutants.

Multigene families have posed an acute problem for evolutionary biologists ever since the revelation that many families exhibit unexpected sequence homogeneity within and between individuals of a species. A family that is shared between several species, in contrast, often reveals substantial heterogeneity between them. This cohesive and species-specific pattern of variation, which disengages from the classical mode of random genetic drift and selection, has been formally described as Molecular Drive (Dover, 1982). Based on initial observations (Cribbs 1982), the tRNA₄Ser and tRUA₇Ser genes on the X-chromosome of Drosophila melaaogaster also showed intriguing characteristics reminiscent of Molecular Drive. However, in this unusual case, the coevolution process would not only encompass the individuals within a family, but would also ensnare members from a different family. This thesis is an in depth study on the concerted evolution of both gene families and provides evidence consistent with the view that they are undergoing Molecular Drive. Eight tRNA₄,₇Ser genes have been cloned from bands 12DE on the X-chromosome of D metanogaster by molecular walking. There are two tRNA₄Ser and two tRNA₇Ser genes that contain sequences expected from their known tRNAs (Cribbs et. al., 1987a). Of the 86 nucleotides, they only differ from each other at positions 16, 34 and 77 (non-standard numbering, see Sprinzl et al., 1987). The difference at position 34 corresponds to the anticodon and accounts for their difference in codon recognition. These genes have been designated as either 444 or 777 genes, based solely on the three diagnostic differences. However, there is also a single 474 and two 774 genes, which are recombinant structures of the bona fide genes. The remaining gene, 444*, has the three nucleotides diagnostic of tRNA₄Ser but contains a mutation at the tip of the extra arm. Thus collectively, the entire caste of tRNA₄,₇Ser genes at 12DE forms a graded series of transitional states, bridging the narrow sequence variability between true tRNA4Ser and tRNA7Ser. Flanking sequences of these hybrid and the 444* genes show segmental homologies related to both the 444 and 777 genes within the cluster, again a strong indication that both gene types are undergoing concerted evolution. Examination of selected genes from two distantly related sibling species, D, erecta and D. yakuba, shows their equivalent flanking sequences have diverged from those of melanogaster. As expected, the base changes in these species, often occurring as clusters, are also non-random and appear to have been propagated to certain respective members to maintain a species-specific and cohesive pattern of variation consistent with Molecular Drive. One possible mode of spreading sequence variation and creating the hybrid genes in the process could involve an initial stage of asymmetric pairing between 444 and 777 DNA. To examine this possibility, a tRNAArg gene cluster also from 12DE was conveniently exploited as independent "monitors". This family shows fluctuations in the number of genes among the different species and strains (Newton, unpublished), which could also be explained by asymmetric pairing of DNA followed by unequal exchange. Thus, even though the tRNAArg and tRNA₄,₇Ser genes have embarked on different evolutionary pathways, both phenomena may be explained by their common susceptibility to local asymmetric pairing of DNA. / Science, Faculty of / Zoology, Department of / Graduate