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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2011) 35, 1233–1238 (Printed in Great Britain)
Gem formation upon constitutive Gemin3 overexpression in Drosophila
Ruben J. Cauchi1
Department of Physiology and Biochemistry, University of Malta, Msida MSD 2080, Malta GC


Gems or ‘Gemini of Cajal bodies’ are spherical nuclear aggregates of SMN (survival of motor neurons) complexes that frequently overlap Cajal bodies. Although described and characterized in mammalian tissues, gems have not been reported in invertebrates. Stimulation of gem formation in the fruitfly Drosophila melanogaster was investigated through the constitutive overexpression of a fluorescently tagged transgene of a DEAD-box SMN complex member, Gemin3, in wild-type tissues. Although expression was predominantly cytoplasmic in the larval brain cells, Gemin3 was found enriched in multiple discrete bright foci in the nuclei of several tissues including epidermis, muscle and gut. Similar to their mammalian counterparts, Drosophila gems contained endogenous SMN and at times overlapped with Cajal bodies. These findings support the hypothesis that gems are storage sites for excess nuclear SMN complexes and their frequent association with Cajal bodies might imply recruitment for nuclear ribonucleoprotein assembly reactions.


Key words: Cajal body, Drosophila, Gemin3, gem, spinal muscular atrophy, survival of motor neurons

Abbreviations: CFP, cyan fluorescent protein, SMA, spinal muscular atrophy, SMN, survival of motor neurons, UAS, upstream activating sequence, RNP, ribonucleoprotein, UsnRNP, uridine-rich small nuclear RNP

1email ruben.cauchi@um.edu.mt


Received 9 March 2011/23 May 2011; accepted 31 May 2011

Published as Cell Biology International Immediate Publication 31 May 2011, doi:10.1042/CBI20110147


© The Author(s) Journal compilation © 2011 Portland Press Limited


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)