Genetic screen identifies a requirement for SMN in mRNA localisation within the Drosophila oocyte.

ABSTRACT:

Objective

Spinal muscular atrophy (SMA) results from insufficient levels of the survival motor neuron (SMN) protein. Drosophila is conducive to large-scale genetic-modifier screens which can reveal novel pathways underpinning the disease mechanism. We tested the ability of a large collection of genomic deletions to enhance SMN-dependent lethality. To test our design, we asked whether our study can identify loci containing genes identified in previous genetic screens. Our objective was to find a common link between genes flagged in independent screens, which would allow us to expose novel functions for SMN in vivo.

Results

Out of 128 chromosome deficiency lines, 12 (9.4%) were found to consistently depress adult viability when crossed to SMN loss-of-function heterozygotes. In

SUBMITTER: Aquilina B 

PROVIDER: S-EPMC5998591 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature