Transcriptional regulation of Drosophila gonad formation
Abstract
The formation of the Drosophila embryonic gonad, involving the fusion of clusters of somatic gonadal precursor cells (SGPs) and their ensheathment of germ cells, provides a simple and genetically tractable model for the interplay between cells during organ formation. In a screen for mutants affecting gonad formation we identified a SGP cell autonomous role for Midline (Mid) and Longitudinals lacking (Lola). These transcriptional factors are required for multiple aspects of SGP behaviour including SGP cluster fusion, germ cell ensheathment and gonad compaction. The lola locus encodes more than 25 differentially spliced isoforms and we have identified an isoform specific requirement for lola in the gonad which is distinct from that in nervous system development. Mid and Lola work in parallel in gonad formation and surprisingly Mid overexpression in a lola background leads to additional SGPs at the expense of fat body cells. Our findings support the idea that although the transcription factors required by SGPs can ostensibly be assigned to those being required for either SGP specification or behaviour, they can also interact to impinge on both processes.
Additional Information
© 2014 Elsevier Inc. Received 3 October 2013, Revised 22 May 2014, Accepted 26 May 2014, Available online 11 June 2014. We thank members of the lab including Jennifer Bergmann, Amrita Mukherjee, Tina Bresser, Kristina Ile and Matthias Schneider for comments on the manuscript. We would also like to thank Uwe Irion for helpful discussion. The lola[C28] and mid[B23] alleles were obtained in a screen for germ cell migration mutants performed in the lab of Ruth Lehmann coordinated by Vitor Barbosa. We acknowledge the DSHB, maintained by The University of Iowa, Department of Biology, as a source of several of the antibodies used in this work. We also acknowledge the Flybase consortium and Bloomington stock centre at Indiana University for gene and stock curation and fly stocks, respectively. We thank the labs of Mark Van Doren, Rolf Reuter, Edward Giniger, Sandra Leal, Dorothea Godt, Manfred Frasch and William Brook for reagents. The authors declare no conflicts of interest.Attached Files
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Additional details
- Eprint ID
- 46439
- DOI
- 10.1016/j.ydbio.2014.05.026
- Resolver ID
- CaltechAUTHORS:20140623-134457638
- Created
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2014-06-23Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field