Disruption of the Pp1-87B Gene Stimulates Tumor Formation in the Eye of Drosophila

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Disruption of the Pp1-87B Gene Stimulates Tumor Formation in the Eye of Drosophila

Journal Title: Annual Research & Review in Biology - Year 2017, Vol 20, Issue 6

Abstract

Protein phosphatases are a set of enzymes in charge of the dephosphorylation of several proteins and enzymes in a cell. Dephosphorylation process is essential for organizing a huge number of cellular actions. In Drosophila, protein phosphatase 1 at B87 (Pp1-87B) gene encodes one of the four variants of the protein phosphatase 1 catalytic subunit and located on chromosome number three of Drosophila melanogaster. In this proposal, Pp1-87B mutation carrying lethal P-element insertions at a third chromosome of Drosophila melanogaster was screened to study the possible of this gene as tumor suppressor gene. Disruption of the genetic sequence of Pp1-87B gene can produce mutant phenotypes in the large clone mosaic eyes. The mutant eyes have either a rough or cell lethal phenotype which indicates the disrupted gene is essential for proper eye development. Further analysis of the mechanism by which these disrupted gene function may offer useful information for cancer studies. To study if the obtained set of Drosophila P-element mutations have a tumorigenic activity or not, a set of somatic clonal analysis in the whole body or in eye system was used. Thus, the lethal mutations were screened in some mosaic assays using clonal analysis systems. Our results showed that the studied gene may have a significant role in eye development, cell proliferation and could be involved in photoreceptor cell patterning, as well as in ommatidial differentiation and apoptosis. This gene which was determined in the present study could have a real impact on cancer development.

Authors and Affiliations

Neima Koutb, A. Abou-Eisha, Adel E. El-Din, S. M. Kassem, Ekram S. Ahmad

Keywords

Pp1-87B gene; P-element insertions; clonal analysis; tumor suppressor gene.

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EP ID EP314982
DOI 10.9734/ARRB/2017/37763
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