196,571 research outputs found
The role of the diamond gene in the control of Drosophila genome stability
No full textDiamond (dind) is an essential Drosophila gene identified by five mutant alleles induced by EMS. Larvae homozygous for these mutations die at the third instar stage due to extensive defects in chromosome structure and mitosis. Cytological analysis of DAPI stained larval brains revealed that in dind mutants dividing cells are arrested in metaphase and exhibit a severe pleiotropic phenotype. 50% of metaphases are aneuploid or polyploid, 2% are endoreduplicated, 65% exhibit irregularly condensed chromosome and 33% contain broken chromosomes. In addition, in dind brains immunostained for tubulin, we consistently observed diploid cells with defective spindles and anaphase-like figures that contain chromosomes with unseparated sister chromatids. The latter defect does not appear to be due to kinetochore defects, as the localization of several kinetochore components is regular in brain cells of dind mutants. Nevertheless, loss of Dind severely compromises chromosome biorentation and segregation. In dind metaphase figures the Spindle Assembly Checkpoint (SAC) component Zw10 accumulates at the kinetochores and does not ‘‘stream’’ along the spindle microtubules, suggesting a failure to satisfy the SAC. Immunostaining of larval brains for the centrosomal and centriolar markers DSpd-2 and Asterless (Asl) revealed that dind mutants exhibit fragmented centrioles surrounded by pericentriolar material (PCM). These centriole-containing centrosomal fragments give rise to aberrant numbers of microtubule organizing centers (MTOCs) that lead to the assembly of disorganized spindles. Analysis of male germline cells revealed that dind mutant spermatogonia and spermatocytes exhibit most of the phenotypic traits observed in somatic cells, pointing to a pleiotropic role of dind in both mitotic and meiotic divisions.
The lethality and the complex mitotic and meiotic phenotypes elicited by dind mutations are completely rescued by the expression of GFP-tagged dind transgenes. The analysis of GFP-Dind and Dind-GFP expressing brains stained with anti-GFP antibodies revealed that Dind has a diffuse localization in both interphase and mitotic cells, with no detectable signal accumulation in any intracellular structure. The same pattern was observed in wild type larval brains immunostained with an anti-Dind antibody. However, Western blotting on larval cell extracts obtained by separation of cytoplasmic, nucleoplasmic and chromatin fractions showed that Dind is present in the fraction deriving from the pelleted nuclear material, suggesting that at least part of the Dind protein is associated with the chromatin throughout most of the cell cycle. We thus investigated possible interactions between Dind and chromosomal proteins whose loss leads to defects similar to those observed in dind mutants such as Separase (Sse) and Topoisomerase 2 (Top2). Both Sse and Top2 levels resulted significantly reduced in brain extracts from dind mutants. Strikingly, also the amount of Dind was lowered in extracts from both Sse and Top2 mutants, pointing to a mutual dependence between Dind and these two chromosomal proteins.
To the best of our knowledge, dind is the first Drosophila gene so far identified specified by mutations that cause the variety of phenotypic traits described here: defects in chromosome condensation, CABs, metaphase arrest, centriole fragmentation, polyploidy, aneuploidy and endoreduplication. The defects in chromosome morphology and integrity might be explained by assuming that loss of Dind alters the chromatin structure, preventing proper recruitment and stability of Sse and Top2, whose loss would in turn destabilize Dind. On the other hand, the metaphase arrest phenotype, the formation of aneuploid and polyploid cells and centriole fragmentation are more difficult to reconcile with a single chromatin-related function of dind. We thus speculate that the unique pleiotropic phenotype of dind mutants is due to the “moonlighting” functions of the Dind protein, which might be able to perform different roles in different contexts. Further experiments will help to verify this hypothesis and elucidate the Dind functions at the molecular level
Heterochromatin and piRNAs in Fragile X mental retardation: insights from Drosophila
No full textFragile X syndrome is a common form of inherited intellectual disability. The mutation responsible for the disease causes the transcriptional silencing of the FMRl gene. It codes for FMRP, an RNA binding protein that is critical for the synaptic plasticity. Studies continue to shed light on the role of FMRP in the neuronal development and to uncover new functions of this protein (Santoro et al., 2012). In this context, Drosophila melanogaster plays an important role as a model for studying the Fragile-X disease and for clarifying all the molecular conserved functions of FMRP. Several studies conducted in Drosophila unveiled the role of FMRP in different small RNA pathways including miRNA and piRNA pathway (Yang et al., 2009; Bozzetti et al., 2015; Specchia et al, 2017).
We will report data showing the role of FMRP in the piRNA pathway in the gonads ensuring the genome stability with a special look at an emerging link between FMRP and HP1. We also present preliminary data showing the presence of the piRNA pathway even in the nervous system suggesting a role of this pathway in the onset of the Fragile-X syndrome
Almost complex manifolds with non-degenerate torsion
No full textWe show that almost complex manifolds (M^4,J) of real dimension 4 for which the image of the Nijenhuis tensor forms a non-integrable bundle, called torsion bundle, admit a Z_2-structure locally, that is, a double absolute parallelism. In this way, the problem of equivalence for such almost complex manifolds can be solved; moreover, the classification of locally homogeneous manifold (M^4,J) is explicitly given when the Lie algebra of its infinitesimal automorphisms is non-solvable (indeed reductive). It is also shown that the group of the automorphisms of (M^4,J) is a Lie group of dimension less than or equal to 4, whose isotropy subgroup has at most two elements, and that there are not non-constant holomorphic functions on (M^4,J)
Dalla culla all'università: l'accidentato percorso educativo dei giovani con background migratorio
No full textIl capitolo, a partire da alcune attività di ricerca condotte nel corso degli ultimi anni, si propone di mettere in luce i percorsi, spesso accidentati, che studenti e studentesse con background migratorio si trovano a vivere nel corso della loro vita. Le scelte educative – sia quelle genitoriali che quelle, in un secondo momento, individuali – rischiano di essere indirizzate, anche istituzionalmente, verso percorsi prestabiliti che rischiano di non conferire all’educazione quel valore di bene pubblico necessario alla costruzione di una società pienamente democratica
Design of an EBG structure by using a transmission line model
No full textAbstract - This paper presents an efficient circuital model based
on a transmission line technique to design a planar circularly
symmetric ERG structure that surrounds a patch antenna
working at 2.45 GHz.
The ERG structure, being printed on the same layer board of the
antenna, is easy to fabricate, prevents the propagation of surface waves and increases the bandwidth and the directivity of the patch antenna
Misleading Issues that Came Up when Calibrating the Alenia Aeronautica Reverberation Chamber
No full text
Università e città: diritti e politiche per la promozione di una piena cittadinanza studentesca
No full textA partire dai dati raccolti tramite il Laboratorio sulla Condizione Abitativa Studentesca HousINgBO, il capitolo intende approfondire tre dimensioni specifiche che rimandano a diritti tra loro distinti ma fortemente interconnessi: il diritto alla casa, il diritto allo studio e il diritto alla salute costituiscono infatti alcuni pre- equisiti fondamentali per la promozione di una piena cittadinanza studentesca, aspetto centrale, da un lato, per studenti e studentesse, così che possano sentirsi parte a pieno titolo della comunità cittadina, ma anche, dall’altro, per la città stessa, la quale riconoscerebbe diritti a protagonisti/e attivi/e dei processi di trasformazione del contesto sociale e urbano, in grado di contribuire ad un arricchimento - non solo economico, ma anche sociale e culturale - del tessuto cittadino. Se la pandemia di Covid-19 ha quindi avuto impatti e conseguenze diverse su una popolazione fortemente differenziata, portando a una ristrutturazione della quotidianità di studenti e studentesse trovatisi a modificare modalità didattiche e relazionali, allo stesso tempo chiama inevitabilmente la
città di Bologna a una serie di riflessioni per immaginare una situazione postpandemica a misura di studente
Stress, transposons and genome evolution
No full textAfter Darwin's book on the origin of species by the natural selection, the theory of his precursor Lamarck was never completely abandoned. Over time, the observation of strange natural phenomena has occasionally resurrected the concept of the heredity of acquired characters. To explain, in Darwinian sense, some of the apparent Lamarckian-like phenomena, Waddington elaborated the “canalization and assimilation” concepts (Waddington, 1959). He observed that some phenotypic traits induced in Drosophila pupae by heat shock treatment and selected for a number of generations in the presence of the same stress, became heritable, thereby showing that an induced phenotypic trait could be inherited trough the germ line. Waddington hypothesized the existence of a cryptic genetic variation that is maintained hidden due to the robustness of the developmental process that he indicated as “canalization”. If an environmental stress is strong enough to overcome this robustness, the development pathway can change because of the expression of a cryptic genetic variant. Then, this variant can be selected and become heritable by an “assimilation” process. During the last few years, data supporting this view and providing possible molecular explanations were published. Rutheford and Lindquist (1998) showed that, in Drosophila, impairment of Hsp90 function induces morphogenetic variants that occasionally became fixed and stably transmitted. The interpretation was that Hsp90 is a capacitor of morphological evolution and buffers a pre-existing genetic variation that is not expressed and accumulates in neutral conditions. The stress sensitive storage and release of genetic variation by Hsp90 would favour adaptive evolution. However, our recent study has suggested a different explanation of these results (Specchia et al., 2010). It has been demonstrated that Hsp90 is involved in repression of transcription and mobilization of transposable elements in germ cells by affecting piRNA biogenesis. The reduction of HSP90 causes stress response-like activation and transposition of mobile elements along with a wide range of phenotypic variants due to the transposon insertions to the corresponding genes. On the basis of these observations, we have suggested that Hsp90, rather than functioning as a capacitor, acts, when absent, as a mutator, capable of causing activation and transposition of mobile elements through impairment of piRNAi silencing. Consequently, we propose that stress causes the activation of transposons that would induce de novo gene mutations, affecting development pathways; mutations can be expressed and fixed across subsequent generations by an assimilation process consisting of a co-selection of a somatic and a germinal event giving the same phenotype. This view implies that transposon activation is a major reaction of genomes to environmental stresses and represents a powerful adaptive response
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