25 research outputs found

    The fate of Arabidopsis thaliana homeologous CNSs and their motifs in the Paleohexaploid Brassica rapa.

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    Following polyploidy, duplicate genes are often deleted, and if they are not, then duplicate regulatory regions are sometimes lost. By what mechanism is this loss and what is the chance that such a loss removes function? To explore these questions, we followed individual Arabidopsis thaliana-A. thaliana conserved noncoding sequences (CNSs) into the Brassica ancestor, through a paleohexaploidy and into Brassica rapa. Thus, a single Brassicaceae CNS has six potential orthologous positions in B. rapa; a single Arabidopsis CNS has three potential homeologous positions. We reasoned that a CNS, if present on a singlet Brassica gene, would be unlikely to lose function compared with a more redundant CNS, and this is the case. Redundant CNSs go nondetectable often. Using this logic, each mechanism of CNS loss was assigned a metric of functionality. By definition, proved deletions do not function as sequence. Our results indicated that CNSs that go nondetectable by base substitution or large insertion are almost certainly still functional (redundancy does not matter much to their detectability frequency), whereas those lost by inferred deletion or indels are approximately 75% likely to be nonfunctional. Overall, an average nondetectable, once-redundant CNS more than 30 bp in length has a 72% chance of being nonfunctional, and that makes sense because 97% of them sort to a molecular mechanism with deletion in its description, but base substitutions do cause loss. Similarly, proved-functional G-boxes go undetectable by deletion 82% of the time. Fractionation mutagenesis is a procedure that uses polyploidy as a mutagenic agent to genetically alter RNA expression profiles, and then to construct testable hypotheses as to the function of the lost regulatory site. We show fractionation mutagenesis to be a deletion machine in the Brassica lineage

    Dose–Sensitivity, Conserved Non-Coding Sequences, and Duplicate Gene Retention through Multiple Tetraploidies in the Grasses

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    Whole genome duplications, or tetraploidies, are an important source of increased gene content. Following whole genome duplication, duplicate copies of many genes are lost from the genome. This loss of genes is biased both in the classes of genes deleted and the subgenome from which they are lost. Many or all classes are genes preferentially retained as duplicate copies are engaged in dose sensitive protein–protein interactions, such that deletion of any one duplicate upsets the status quo of subunit concentrations, and presumably lowers fitness as a result. Transcription factors are also preferentially retained following every whole genome duplications studied. This has been explained as a consequence of protein–protein interactions, just as for other highly retained classes of genes. We show that the quantity of conserved noncoding sequences (CNSs) associated with genes predicts the likelihood of their retention as duplicate pairs following whole genome duplication. As many CNSs likely represent binding sites for transcriptional regulators, we propose that the likelihood of gene retention following tetraploidy may also be influenced by dose–sensitive protein–DNA interactions between the regulatory regions of CNS-rich genes – nicknamed bigfoot genes – and the proteins that bind to them. Using grass genomes, we show that differential loss of CNSs from one member of a pair following the pre-grass tetraploidy reduces its chance of retention in the subsequent maize lineage tetraploidy

    Pearl millet genome sequence provides a resource to improve agronomic traits in arid environments

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    Pearl millet [Pennisetum glaucum (L.) R. Br., syn. Cenchrus americanus (L.) Morrone], is a staple food for over 90 million poor farmers in arid and semi-arid regions of sub-Saharan Africa and South Asia. We report the ~1.79 Gb genome sequence of reference genotype Tift 23D2B1-P1-P5, which contains an estimated 38,579 genes. Resequencing analysis of 994 (963 inbreds of the highly cross-pollinated cultigen, and 31 wild accessions) provides insights into population structure, genetic diversity, evolution and domestication history. In addition we demonstrated the use of re-sequence data for establishing marker trait associations, genomic selection and prediction of hybrid performance and defining heterotic pools. The genome wide variations and abiotic stress proteome data are useful resources for pearl millet improvement through deploying modern breeding tools for accelerating genetic gains in pearl millet.publishersversionPeer reviewe

    Studies on the expression of synaptic terminal proteins and neurotransmitter receptors in the rat brain following amphetamine-induced behavioral sensitization

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    This study investigated alteration in the expression of syntaxin1, synaptophysin and synapsin1, synaptic proteins involved in neurotransmitter release/synaptic plasticity. The results of this study indicated significant reduction in the expression of syntaxin I and synaptophysin in the core subregion of the nucleus accumbens along with a significant enhancement in syntaxin I expression in the shell subregion. Thus repeated administration of amphetamine induced differential changes in synaptic protein expression between the core and shell subregions of the nucleus accumbens. This result is consistent with several studies reporting differential neurochemical changes occurring in the core and shell in response to repeated psychostimulant administration (Cadoni and Di Chiara, 1999; 2000; Cadoni et al., 2000).This study also investigated possible alteration in glutamatergic (NMDA and kainate) and dopaminergic (D3) receptor levels in response to amphetamine-induced behavioral sensitization. The results of this study indicated a lack of significant difference in the expression of these receptors following amphetamine sensitization. (Abstract shortened by UMI.

    Supplementary table II

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    <p>Orphans in all three subgenomes in <em>Br</em></p

    Chapter 4

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    <p>chapter 4 suppl data</p

    VEGI CNSs MF CNSs Comparison

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    <p>VEGI CNSs MF CNSs Comparison</p
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