GAGA Regulates Border Cell Migration in <i>Drosophila</i>

• Main Authors: Anna A. Ogienko, Lyubov A. Yarinich, Elena V. Fedorova, Natalya V. Dorogova, Sergey I. Bayborodin, Elina M. Baricheva, Alexey V. Pindyurin
• Format: Article
• Language: English
• Published: MDPI AG 2020-10-01
• Series: International Journal of Molecular Sciences
• Subjects: Drosophila melanogaster; cell migration; border cells; slbo; Trl; GAGA
• Online Access: https://www.mdpi.com/1422-0067/21/20/7468
• ISSN: 1661-6596; 1422-0067

Collective cell migration is a complex process that happens during normal development of many multicellular organisms, as well as during oncological transformations. In <i>Drosophila</i> oogenesis, a small set of follicle cells originally located at the anterior tip of each egg chamber become motile and migrate as a cluster through nurse cells toward the oocyte. These specialized cells are referred to as border cells (BCs) and provide a simple and convenient model system to study collective cell migration. The process is known to be complexly regulated at different levels and the product of the <i>slow border cells</i> (<i>slbo</i>) gene, the C/EBP transcription factor, is one of the key elements in this process. However, little is known about the regulation of <i>slbo</i> expression. On the other hand, the ubiquitously expressed transcription factor GAGA, which is encoded by the <i>Trithorax</i><i>-like</i> (<i>Trl</i>) gene was previously demonstrated to be important for <i>Drosophila</i> oogenesis. Here, we found that <i>Trl</i> mutations cause substantial defects in BC migration. Partially, these defects are explained by the reduced level of <i>slbo</i> expression in BCs. Additionally, a strong genetic interaction between <i>Trl</i> and <i>slbo</i> mutants, along with the presence of putative GAGA binding sites within the <i>slbo</i> promoter and enhancer, suggests the direct regulation of this gene by GAGA. This idea is supported by the reduction in the <i>slbo</i>-Gal4-driven GFP expression within BC clusters in <i>Trl</i> mutant background. However, the inability of <i>slbo</i> overexpression to compensate defects in BC migration caused by <i>Trl</i> mutations suggests that there are other GAGA target genes contributing to this process. Taken together, the results define GAGA as another important regulator of BC migration in <i>Drosophila</i> oogenesis.