Abstract
Mini chromosome maintenance 10 (Mcm10) is an essential protein, which is conserved from S. cerevisiae to Drosophila and human, and is required for the initiation of DNA replication. Knockdown of Drosophila Mcm10 (dMcm10) by RNA interference in eye imaginal discs induces abnormal eye morphology (rough eye phenotype), and the number of ommatidia is decreased in adult eyes. We also observed a delay in the S phase and M phase in eye discs of dMcm10 knockdown fly lines. These results show important roles for dMcm10 in the progression of S and M phases. Furthermore, genome damage and apoptosis were induced by dMcm10 knockdown in eye imaginal discs. Surprisingly, when we used deadpan-lacZ and klingon-lacZ enhancer trap lines to monitor the photoreceptor cells in eye discs, knockdown of dMcm10 by the GMR-GAL4 driver reduced the signals of R7 photoreceptor cells. These data suggest an involvement of dMcm10 in R7 cell differentiation. This involvement appears to be independent of the apoptosis induced by dMcm10 knockdown. Together, these results suggest that dMcm10 knockdown has an effect on DNA replication and R7 cell differentiation.
Highlights
Minichromosome maintenance protein 10 (Mcm10) is needed for DNA replication in eukaryotes [1,2,3,4,5,6]
These results indicate that the anti-Drosophila Mcm10 (dMcm10) antibody can detect dMcm10 protein, and confirmed that the RNAi line shows an efficient knockdown of dMcm10
Mcm10 was initially identified as a protein with a role in DNA replication, functions of Mcm10 in different cellular processes have been suggested [17,23,24]
Summary
Minichromosome maintenance protein 10 (Mcm10) is needed for DNA replication in eukaryotes [1,2,3,4,5,6]. Recent in vitro studies in yeast have shown that the recruitment of Mcm to the origin occurs after the assembly of the Cdc45-Mcm2-7-GINS complex (CMG) [4,5] Consistent with this latter model, two other in vivo studies demonstrated that Cdc loading onto chromatin was independent of Mcm10 [2,7]. Some groups have suggested that Mcm works as an active helicase activator [8], while others have demonstrated its role as a facilitator of single stranded DNA (ssDNA) binding [9,10] In the former model, Mcm may act to release one DNA strand from the core of CMG complex at the origin, and assist the translocase activity in the 39 to 59 direction resulting in origin unwinding and replication initiation. In the latter model, after the active CMG complex unwinds the origin of replication, Mcm may stabilize the formation of ssDNA via its ssDNA-binding domain in order to initiate DNA replication
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
