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Background  DEAD-box RNA helicase Gemin3 is an essential protein since its deficiency is lethal in both vertebrates and invertebrates. In addition to playing a role in transcriptional regulation and RNA silencing, as a core member of the SMN (survival of motor neurons) complex, Gemin3 is required for the biogenesis of spliceosomal snRNPs (small nuclear ribonucleoproteins), and axonal mRNA metabolism. Studies in the mouse and C.  elegans  revealed that loss of Gemin3 function has a negative impact on ovarian physiology and development.    Findings  This work reports on the generation and characterisation of  gemin3  mutant germline clones in  Drosophila  adult females. Gemin3 was found to be required for the completion of oogenesis and its loss led to egg polarity defects, oocyte mislocalisation, and abnormal chromosome morphology. Canonical Cajal bodies were absent in the majority of  gemin3  mutant egg chambers and histone locus bodies displayed an atypical morphology. snRNP distribution was perturbed so that on  gemin3  loss, snRNP cytoplasmic aggregates (U bodies) were only visible in wild type.    Conclusions  These findings establish a conserved requirement for Gemin3 in  Drosophila  oogenesis. Furthermore, in view of the similarity to the phenotypes described previously in  smn  mutant germ cells, the present results confirm the close functional relationship between SMN and Gemin3 on a cellular level.

Conserved requirement for DEAD-box RNA helicase Gemin3 in Drosophila oogenesis