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    High-content RNAi screening identifies the Type 1 inositol triphosphate receptor as a modifier of TDP-43 localization and neurotoxicity (2012)
    Oxford University Press
    Details
    Publication Date: 2012-10-26
    Description: Cytosolic aggregation of the nuclear RNA-binding protein (RBP) TDP-43 (43 kDa TAR DNA-binding domain protein) is a suspected direct or indirect cause of motor neuron deterioration in amyotrophic lateral sclerosis (ALS). In this study, we implemented a high-content, genome-wide RNAi screen to identify pathways controlling TDP-43 nucleocytoplasmic shuttling. We identified ~60 genes whose silencing increased the cytosolic localization of TDP-43, including nuclear pore complex components and regulators of G2/M cell cycle transition. In addition, we identified the type 1 inositol-1,4,5-trisphosphate (IP3) receptor (ITPR1), an IP3-gated, endoplasmic reticulum (ER)-resident Ca 2+ channel, as a strong modulator of TDP-43 nucleocytoplasmic shuttling. Knockdown or chemical inhibition of ITPR1 induced TDP-43 nuclear export in immortalized cells and primary neurons and strongly potentiated the recruitment of TDP-43 to Ubiquilin-positive autophagosomes, suggesting that diminished ITPR1 function leads to autophagosomal clearance of TDP-43. The functional significance of the TDP-43-ITPR1 genetic interaction was tested in Drosophila , where mutant alleles of ITPR1 were found to significantly extended lifespan and mobility of flies expressing TDP-43 under a motor neuron driver. These combined findings implicate IP3-gated Ca 2+ as a key regulator of TDP-43 nucleoplasmic shuttling and proteostasis and suggest pharmacologic inhibition of ITPR1 as a strategy to combat TDP-43-induced neurodegeneration in vivo .
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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    Recently formed polyploid plants diversify at lower rates (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-08-20
    Description: Polyploidy, the doubling of genomic content, is a widespread feature, especially among plants, yet its macroevolutionary impacts are contentious. Traditionally, polyploidy has been considered an evolutionary dead end, whereas recent genomic studies suggest that polyploidy has been a key driver of macroevolutionary success. We examined the consequences of polyploidy on the time scale of genera across a diverse set of vascular plants, encompassing hundreds of inferred polyploidization events. Likelihood-based analyses indicate that polyploids generally exhibit lower speciation rates and higher extinction rates than diploids, providing the first quantitative corroboration of the dead-end hypothesis. The increased speciation rates of diploids can, in part, be ascribed to their capacity to speciate via polyploidy. Only particularly fit lineages of polyploids may persist to enjoy longer-term evolutionary success.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayrose, Itay -- Zhan, Shing H -- Rothfels, Carl J -- Magnuson-Ford, Karen -- Barker, Michael S -- Rieseberg, Loren H -- Otto, Sarah P -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1257. doi: 10.1126/science.1207205. Epub 2011 Aug 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biodiversity Research Centre, University of British Columbia, Vancouver, BC V6T 1Z4, Canada. itaymay@post.tau.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852456" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/*genetics ; *Biological Evolution ; Diploidy ; *Extinction, Biological ; Ferns/*genetics ; *Genetic Speciation ; Genome, Plant ; *Polyploidy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Molecular Evolution across the Asteraceae: Micro- and Macroevolutionary Processes (2011)
    Oxford University Press
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    Publication Date: 2011-06-20
    Print ISSN: 0737-4038
    Electronic ISSN: 1537-1719
    Topics: Biology
    Published by Oxford University Press
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