dictyNews
Electronic Edition
Volume 37, number 2
July 22, 2011

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=========
Abstracts
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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 [[log in to unmask]]
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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 [[log in to unmask]]
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[End dictyNews, volume 37, number 2]