112 research outputs found

    Heterochromatin: A Rapidly Evolving Species Barrier

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    Recent work has shown that changes in the sequence composition of heterochromatin, or in the factors that maintain that heterochromatin, may play an important role in speciation

    The Inhibition of Polo Kinase by Matrimony Maintains G2 Arrest in the Meiotic Cell Cycle

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    Many meiotic systems in female animals include a lengthy arrest in G2 that separates the end of pachytene from nuclear envelope breakdown (NEB). However, the mechanisms by which a meiotic cell can arrest for long periods of time (decades in human females) have remained a mystery. The Drosophila Matrimony (Mtrm) protein is expressed from the end of pachytene until the completion of meiosis I. Loss-of-function mtrm mutants result in precocious NEB. Coimmunoprecipitation experiments reveal that Mtrm physically interacts with Polo kinase (Polo) in vivo, and multidimensional protein identification technology mass spectrometry analysis reveals that Mtrm binds to Polo with an approximate stoichiometry of 1:1. Mutation of a Polo-Box Domain (PBD) binding site in Mtrm ablates the function of Mtrm and the physical interaction of Mtrm with Polo. The meiotic defects observed in mtrm/+ heterozygotes are fully suppressed by reducing the dose of polo+, demonstrating that Mtrm acts as an inhibitor of Polo. Mtrm acts as a negative regulator of Polo during the later stages of G2 arrest. Indeed, both the repression of Polo expression until stage 11 and the inactivation of newly synthesized Polo by Mtrm until stage 13 play critical roles in maintaining and properly terminating G2 arrest. Our data suggest a model in which the eventual activation of Cdc25 by an excess of Polo at stage 13 triggers NEB and entry into prometaphase

    The “conscious pilot”—dendritic synchrony moves through the brain to mediate consciousness

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    Cognitive brain functions including sensory processing and control of behavior are understood as “neurocomputation” in axonal–dendritic synaptic networks of “integrate-and-fire” neurons. Cognitive neurocomputation with consciousness is accompanied by 30- to 90-Hz gamma synchrony electroencephalography (EEG), and non-conscious neurocomputation is not. Gamma synchrony EEG derives largely from neuronal groups linked by dendritic–dendritic gap junctions, forming transient syncytia (“dendritic webs”) in input/integration layers oriented sideways to axonal–dendritic neurocomputational flow. As gap junctions open and close, a gamma-synchronized dendritic web can rapidly change topology and move through the brain as a spatiotemporal envelope performing collective integration and volitional choices correlating with consciousness. The “conscious pilot” is a metaphorical description for a mobile gamma-synchronized dendritic web as vehicle for a conscious agent/pilot which experiences and assumes control of otherwise non-conscious auto-pilot neurocomputation

    The elegans of spindle assembly

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    The Caenorhabditis elegans one-cell embryo is a powerful system in which to study microtubule organization because this large cell assembles both meiotic and mitotic spindles within the same cytoplasm over the course of 1 h in a stereotypical manner. The fertilized oocyte assembles two consecutive acentrosomal meiotic spindles that function to reduce the replicated maternal diploid set of chromosomes to a single-copy haploid set. The resulting maternal DNA then unites with the paternal DNA to form a zygotic diploid complement, around which a centrosome-based mitotic spindle forms. The early C. elegans embryo is amenable to live-cell imaging and electron tomography, permitting a detailed structural comparison of the meiotic and mitotic modes of spindle assembly

    Adaptive evolution targets a piRNA precursor transcription network

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    File "cuff cDNA sequences.docx" contains cloned cuff cDNA sequences from Drosophila melanogaster and Drosophila simulans used to make transgenes.Files "nG_Cuff_proteomics" and "rhiP_Cuff_proteomics" are scaffold files, which contains mass spectrometry protein spectrum counts for Cuff immuno-precipitates. Cuff proteins are either driven by rhi promoter (rhiP) or UASp promoter under nos-Gal4 driver (nG). These files can be opened by Scaffold Protein Spectra Viewer by Proteome Software

    Adaptive evolution targets a piRNA precursor transcription network

    No full text
    File "cuff cDNA sequences.docx" contains cloned cuff cDNA sequences from Drosophila melanogaster and Drosophila simulans used to make transgenes.Files "nG_Cuff_proteomics" and "rhiP_Cuff_proteomics" are scaffold files, which contains mass spectrometry protein spectrum counts for Cuff immuno-precipitates. Cuff proteins are either driven by rhi promoter (rhiP) or UASp promoter under nos-Gal4 driver (nG). These files can be opened by Scaffold Protein Spectra Viewer by Proteome Software.THIS DATASET IS ARCHIVED AT DANS/EASY, BUT NOT ACCESSIBLE HERE. TO VIEW A LIST OF FILES AND ACCESS THE FILES IN THIS DATASET CLICK ON THE DOI-LINK ABOV

    Adaptive evolution leads to cross-species incompatibility in the piRNA transposon silencing machinery

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    Contains mass spectrometry scaffold files for immuno-precipitated samples and also cloned rhi and del gene sequences used in this stud

    DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos

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    During early embryogenesis of Drosophila melanogaster, mutations in the DNA-replication checkpoint lead to chromosome-segregation failures. Here we show that these segregation failures are associated with the assembly of an anastral microtubule spindle, a mitosis-specific loss of centrosome function, and dissociation of several components of the gamma-tubulin ring complex from a core centrosomal structure. The DNA-replication inhibitor aphidicolin and DNA-damaging agents trigger identical mitotic defects in wild-type embryos, indicating that centrosome inactivation is a checkpoint-independent and mitosis-specific response to damaged or incompletely replicated DNA, We propose that centrosome inactivation is part of a damage-control system that blocks chromosome segregation when replication/damage checkpoint control fails
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