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Drosophila protein GAGA (GAF) is a factor of epigenetic transcription regulation of a large group of genes with a wide variety of cellular functions. GAF is encoded by the Trithorax-like (Trl) gene, which is important for the formation of various organs and tissues at all stages of ontogenesis. In our previous works, we showed that this protein is necessary for the development of the reproductive system, both in males and females of Drosophila. Decreased expression of the Trl gene led to multiple disorders of spermatogenesis and oogenesis. One of the significant disorders was associated with massive degradation and loss of cells in the germline. In this work, we carried out a more detailed cytological study to determine what type of germ cell death is characteristic of Trl mutants, and whether there are disturbances or changes in this process compared to the norm. The results obtained showed that the lack of GAF protein causes massive germ cell death in both females and males of Drosophila, but this death manifests itself in different ways, depending on the sex. In Trl females, this process does not differ phenotypically from the norm. In the dying egg chambers, signs of apoptosis and autophagy were revealed, as well as morphological features that are characteristic of the wild type. In males, Trl mutations induce mass germ cell death through autophagy, which is not typical of Drosophila spermatogenesis, and has not been previously described, neither in the norm nor in other genes’ mutations. Thus, GAF lack in Trl mutants leads to increased germ cell death through apoptosis and autophagy. Ectopic cell death and germ line atrophy are probably associated with impaired expression of the GAGA factor target genes, among which there are genes that regulate both apoptosis and autophagy.

Cell migration is an important morphogenetic process necessary at different stages of individual development and body functioning. The initiation and maintenance of the cell movement state requires the activation of many factors involved in the regulation of transcription, signal transduction, adhesive interactions, modulation of membranes and the cytoskeleton. However, cell movement depends on the status of both migrating and surrounding cells, interacting with each other during movement. The surrounding cells or cell matrix not only form a substrate for movement, but can also participate in the spatio-temporal regulation of the migration. At present, there is no exact understanding of the genetic mechanisms of this regulation. To determine the role of the cell environment in the regulation of individual cell migration, we studied the migration of primordial germline cells (PGC) during early embryogenesis in Drosophila melanogaster. Normally, PGC are formed at the 3rd stage of embryogenesis at the posterior pole of the embryo. During gastrulation (stages 6–7), PGC as a consolidated cell group passively transfers into the midgut primordium. Further, PGC are individualized, acquire an amoeboid form, and actively move through the midgut epithelium and migrate to the 5–6 abdominal segment of the embryo, where they form paired embryonic gonads. We screened for genes expressed in the epithelium surrounding PGC during early embryogenesis and affecting their migration. We identified the myc, Hph, stat92E, Tre-1, and hop genes, whose RNA interference leads to premature active PGC migration at stages 4–7 of embryogenesis. These genes can be divided into two groups: 1) modulators of JAK/STAT pathway activity inducing PGC migration (stat92E, Tre-1, hop), and 2) myc and Hph involved in epithelial morphogenesis and polarization, i.e. modifying the permeability of the epithelial barrier. Since a depletion of each of these gene products resulted in premature PGC migration, we can conclude that, normally, the somatic environment negatively regulates PGC migration during early Drosophila embryogenesis.

The Drosophila melanogaster pAbp gene encodes the cytoplasmic poly(A)-binding protein (PABP). Cytoplasmic PABPs participate in the metabolic pathways of the mRNA: translation initiation and termination, cytoplasmic polyadenylation/deadenylation, mRNA stability, mRNA degradation. Despite the extensive biochemical and structural characterization, relatively little is known about the biological roles of PABPs in the processes of cellular development and differentiation. In Drosophila spermatogenesis, posttranscriptional mechanisms of gene regulation play an important role, so cytoplasmic PABP can have significant function in this process. Deletion of PABP leads to embryonic lethality. However, some flies carrying combinations of mutant pAbp alleles survive but display male sterility and show defects in spermatogenesis. It has previously been shown that hypomorphic pAbp mutations cause a number of meiotic defects, abnormalities of Nebenkern formation. These data provide an insight into the effect of pAbp mutation on the individual events of spermatogenesis, but they do not cover the entire process. We studied spermatogenesis in pAbpallele heterozygotes by transmission electron and fluorescent light microscopy. We showed that cellular mitochondria were the primary structural target of the mutation. Abnormal mitochondria were less structured, swollen, had transparent matrix and depleted cristae. Further mutation had a polymorphous effect and induced anomalies in the ultrastructure of mature spermatocytes, defects in Nebenkern formation and division, axial complex formation, shutdown of spermatogenesis during spermatid elongation. Thus our data show a significant role of PABP in structural transformations of male germ cells during entire spermato-genesis.