29 research outputs found
The Drosophila simulans Genome Lacks the crystal-Stellate System
The cry-Ste system is a genetic interaction system between heterochromatin and euchromatin in Drosophila melanogaster, regulated via the piRNA pathway. Deregulation of this system leads to meiotic defects and male sterility. Although the cry-Ste system is peculiar to D. melanogaster, ancestors of Ste and Su(Ste) elements are present in the three closely related species, D. simulans, D. sechellia, and D. mauritiana. The birth, evolution, and maintenance of this genetic system in Drosophila melanogaster are of interest. We investigate the presence of sequences homologous to cry and Ste elements in the simulans complex and describe their chromosomal distribution. The organization and expression of cry- and Ste-like sequences were further characterized in the D. simulans genome. Our results allow us to conclude that the cry-Ste genetic interaction system is absent in the D. simulans genome
Drosophilidae monitoring in Apulia (Italy) reveals Drosophila suzukii as one of the four most abundant species
The knowledge of the endemic drosophilid assemblage is a useful reference to study population dynamics when new species are
introduced in a geographical area. The introduction of invasive species can change the structure of the drosophilid community;
hence, the distribution data for endemic species are also essential to support efficient pest management. We provide the first description
of the natural drosophilid populations (Diptera Drosophilidae) recorded in Apulia, in Southern Italy. The flies, which
were collected in a field survey throughout a year, were classified by morphological and molecular analyses by sequencing the
barcode fragment of the COI mtDNA gene. The identified species show a distribution of frequencies that varies throughout the
year, reflecting a seasonal life cycle peculiar to each species. Among the recorded drosophilids, the potential pest species Drosophila
suzukii represents one of the four most abundant species
Drosophilidae monitoring in Apulia (Italy) reveals Drosophila suzukii as one of the four most abundant species
The knowledge of the endemic drosophilid assemblage is a useful reference to study population dynamics when new species are introduced in a geographical area. The introduction of invasive species can change the structure of the drosophilid community; hence, the distribution data for endemic species are also essential to support efficient pest management. We provide the first description of the natural drosophilid populations (Diptera Drosophilidae) recorded in Apulia, in Southern Italy. The flies, which were collected in a field survey throughout a year, were classified by morphological and molecular analyses by sequencing the barcode fragment of the COI mtDNA gene. The identified species show a distribution of frequencies that varies throughout the year, reflecting a seasonal life cycle peculiar to each species. Among the recorded drosophilids, the potential pest species Drosophila suzukii represents one of the four most abundant species
The “special” crystal-Stellate system in Drosophila melanogaster reveals mechanisms underlying piRNA pathway-mediated canalization
The Stellate-made crystals formation in spermatocytes is the phenotypic manifestation of a disrupted crystal-Stellate interaction
in testes of Drosophila melanogaster. Stellate silencing is achieved by the piRNA pathway, but many features still remain unknown.
Here we outline the important role of the crystal-Stellate modifiers. These have shed light on the piRNA pathways that defend
genome integrity against transposons and other repetitive elements in the gonads. In particular, we illustrate the finding that HSP90
participates in the molecular pathways of piRNA production. This observation has relevance for the mechanisms underlying the
evolutionary canalization process
Hsp90 prevents phenotypic variation by suppressing the mutagenic activity of transposons
The canalization concept(1) describes the resistance of a developmental process to phenotypic variation, regardless of genetic and environmental perturbations, owing to the existence of buffering mechanisms. Severe perturbations, which overcome such buffering mechanisms, produce altered phenotypes that can be heritable and can themselves be canalized by a genetic assimilation process. An important implication of this concept is that the buffering mechanism could be genetically controlled. Recent studies on Hsp90, a protein involved in several cellular processes and development pathways(2-5), indicate that it is a possible molecular mechanism for canalization and genetic assimilation. In both flies and plants, mutations in the Hsp90-encoding gene induce a wide range of phenotypic abnormalities, which have been interpreted as an increased sensitivity of different developmental pathways to hidden genetic variability(6,7.) Thus, Hsp90 chaperone machinery may be an evolutionarily conserved buffering mechanism of phenotypic variance, which provides the genetic material for natural selection. Here we offer an additional, perhaps alternative, explanation for proposals of a concrete mechanism underlying canalization. We show that, in Drosophila, functional alterations of Hsp90 affect the Piwi-interacting RNA (piRNA; a class of germ-line-specific small RNAs) silencing mechanism leading to transposon activation and the induction of morphological mutants. This indicates that Hsp90 mutations can generate new variation by transposon-mediated 'canonical' mutagenesis
Structure, regulation and evolution of the crystal-Stellate system of Drosophila
The crystal-Stellate system is one of the most known example of interaction between heterochromatin and euchromatin: a heterochromatic locus on the Y chromosome (crystal) 'represses' a euchromatic locus (Stellate) on the X chromosome in Drosophila melanogaster. The molecular mechanism regulating this interaction is not completely understood. It is becoming clear that an RNA interference (RNAi) mechanism could be responsible for the silencing carried out by crystal on the Stellate sequences. Here, a detailed structural analysis of all the sequences involved in the system is reported, demonstrating a their 'puzzling' structure. In addition three autosomal mutations: sting, scratch and sirio are described that interfere with the system. All of them are male sterile mutations and exhibit crystals made by the STELLATE protein in their primary spermatocytes. They are requested during oogenesis and early in embryogenesis as well. Hypothesis on the involvement of these genes in activating the Stellate sequences are discussed
Roles for piRNA-related genes in the silencing of repetitive sequences and transposons in gonads of Drosophila melanogaster
GENETIC CHARACTERIZATION OF KNOWN AND NOVEL COMPONENTS OF PIRNA PATHWAYS IN DROSOPHILA MELANOGASTER GONADS
Loss of Pol32 in Drosophila melanogaster Causes Chromosome Instability and Suppresses Variegation
Pol32 is an accessory subunit of the replicative DNA Polymerase delta and of the translesion Polymerase zeta. Pol32 is involved in DNA replication, recombination and repair. Pol32's participation in high-and low-fidelity processes, together with the phenotypes arising from its disruption, imply multiple roles for this subunit within eukaryotic cells, not all of which have been fully elucidated. Using pol32 null mutants and two partial loss-of-function alleles pol32(rd1) and pol32(rds) in Drosophila melanogaster, we show that Pol32 plays an essential role in promoting genome stability. Pol32 is essential to ensure DNA replication in early embryogenesis and it participates in the repair of mitotic chromosome breakage. In addition we found that pol32 mutantssuppress position effect variegation, suggesting a role for Pol32 in chromatin architecture
Loss of Pol32 in Drosophila melanogaster causes chromosome instability and suppresses variegation
Pol32 is an accessory subunit of the replicative DNA Polymerase δ and of the translesion Polymerase ζ. Pol32 is involved in DNA replication, recombination and repair. Pol32's participation in high- and low-fidelity processes, together with the phenotypes arising from its disruption, imply multiple roles for this subunit within eukaryotic cells, not all of which have been fully elucidated. Using pol32 null mutants and two partial loss-of-function alleles pol32rd1 and pol32rds in Drosophila melanogaster, we show that Pol32 plays an essential role in promoting genome stability. Pol32 is essential to ensure DNA replication in early embryogenesis and it participates in the repair of mitotic chromosome breakage. In addition we found that pol32 mutants suppress position effect variegation, suggesting a role for Pol32 in chromatin architecture
