dictyNews Electronic Edition Volume 37, number 2 July 22, 2011 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to dicty@northwestern.edu or by using the form at http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit. Back issues of dictyNews, the Dicty Reference database and other useful information is available at dictyBase - http://dictybase.org. Follow dictyBase on twitter: http://twitter.com/dictybase ========= Abstracts ========= Defective ribosome assembly in Shwachman-Diamond syndrome Chi C. Wong1, 2, David Traynor1, Nicolas Basse1, 2, Robert R. Kay1, Alan J. Warren1, 2 1MRC Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 0QH, UK. 2The Department of Haematology, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK. Blood, In press. Shwachman-Diamond syndrome (SDS), a recessive leukemia predisposition disorder characterized by bone marrow failure, exocrine pancreatic insufficiency, skeletal abnormalities and poor growth, is caused by mutations in the highly conserved SBDS gene. Here, we test the hypothesis that defective ribosome biogenesis underlies the pathogenesis of SDS. We create conditional mutants in the essential SBDS ortholog of the ancient eukaryote Dictyostelium discoideum using temperature-sensitive, self-splicing inteins, showing that mutant cells fail to grow at the restrictive temperature because ribosomal subunit joining is markedly impaired. Remarkably, wild type human SBDS complements the growth and ribosome assembly defects in mutant Dictyostelium cells, but disease-associated human SBDS variants are defective. SBDS directly interacts with the GTPase elongation factor-like 1 (EFL1) on nascent 60S subunits in vivo and together they catalyze eviction of the ribosome anti-association factor eukaryotic initiation factor 6 (eIF6), a prerequisite for the translational activation of ribosomes. Importantly, lymphoblasts from SDS patients harbor a striking defect in ribosomal subunit joining whose magnitude is inversely proportional to the level of SBDS protein. These findings in Dictyostelium and SDS patient cells provide compelling support for the hypothesis that SDS is a ribosomopathy caused by corruption of an essential cytoplasmic step in 60S subunit maturation. Submitted by: Alan Warren [ajw@mrc-lmb.cam.ac.uk] -------------------------------------------------------------------------------- Phototaxis: Microbial Claire Y Allan and Paul R Fisher Department of Microbiology, La Trobe University, Melbourne, VIC 3086, Australia Encyclopedia of Life Sciences, In press Phototaxis in its broadest sense is light-regulated movement of motile organisms (microorganisms in the case of microbial phototaxis), usually resulting in their attraction to (positive phototaxis) or avoidance of (negative phototaxis) illuminated regions. Prokaryotes often use a time-biased random walk strategy under which they choose directions randomly, but move for longer time periods in the chosen direction when that direction happens to be correct. They employ type I sensory rhodopsin photoreceptors and two-component histidine kinase-mediated phosphotransfer systems to regulate flagellar movement. Eukaryotic microbes by contrast can sense and respond to the direction of light by regulating the direction of movement. Phototransduction pathways in eukaryotic microbes appear to involve protein phosphorylation/dephosphorylation at serine or threonine residues, and the responsible kinases and phosphatases are regulated by second messengers. This review focuses on select representative organisms from each of the three taxonomic domains whose photosensory signal transduction pathways have been studied. Although many components of the signal transduction pathways controlling phototaxis have been identified, there is still much to be elucidated. Submitted by Paul Fisher [P.Fisher@latrobe.edu.au] ============================================================== [End dictyNews, volume 37, number 2]