Drosophila p115 is required for Cdk1 activation and G2/M cell cycle transition

• Published in: Mechanisms of development Vol. 144; no. Pt B; pp. 191 - 200
• Main Authors: Ibar, Consuelo, Glavic, Álvaro
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.04.2017
• Subjects: Animals; CDC2 Protein Kinase - metabolism; Cdk1; Cell cycle; Cell Proliferation; Drosophila; Drosophila melanogaster - cytology; Drosophila melanogaster - enzymology; Drosophila melanogaster - growth & development; Drosophila Proteins - metabolism; Drosophila Proteins - physiology; Enzyme Activation; Exocytosis; Female; G2 Phase Cell Cycle Checkpoints; Gene Expression; Golgi; M Phase Cell Cycle Checkpoints; Membrane Proteins - physiology; p115; Wings, Animal - growth & development; Cdk1; Golgi; Drosophila; p115; Cell cycle
• ISSN: 0925-4773; 1872-6356
• DOI: 10.1016/j.mod.2017.04.001

Golgi complex inheritance and its relationship with the cell cycle are central in cell biology. Golgi matrix proteins, known as golgins, are one of the components that underlie the shape and functionality of this organelle. In mammalian cells, golgins are phosphorylated during mitosis to allow fragmentation of the Golgi ribbon and they also participate in spindle dynamics; both processes are required for cell cycle progression. Little is known about the function of golgins during mitosis in metazoans in vivo. This is particularly significant in Drosophila, in which the Golgi architecture is distributed in numerous units scattered throughout the cytoplasm, in contrast with mammalian cells. We examined the function of the ER/cis-Golgi golgin p115 during the proliferative phase of the Drosophila wing imaginal disc. Knockdown of p115 decreased tissue size. This phenotype was not caused by programmed cell death or cell size reductions, but by a reduction in the final cell number due to an accumulation of cells at the G2/M transition. This phenomenon frequently allows mitotic bypass and re-replication of DNA. These outcomes are similar to those observed following the partial loss of function of positive regulators of Cdk1 in Drosophila. In agreement with this, Cdk1 activation was reduced upon p115 knockdown. Interestingly, these phenotypes were fully rescued by Cdk1 overexpression and partially rescued by Myt1 depletion, but not by String (also known as Cdc25) overexpression. Additionally, we confirmed the physical interaction between p115 and Cdk1, suggesting that the formation of a complex where both proteins are present is essential for the full activation of Cdk1 and thus the correct progression of mitosis in proliferating tissues. •Knockdown of p115 causes a decrease of Drosophila wing size.•Cells are retained in mitotic G2/M transition and have defects in spindle formation.•Cdk1 activation is reduced and wing phenotypes are rescued by Cdk1 overexpression.•Cdk1 physically interacts with p115.•p115 is required for mitosis progression in proliferating tissues.