Overcoming Centrosome Duplication Defects by the SESA Network

Abstract

Thecorrect separation of chromosomes during mitosis is necessary to preventgenetic instability and aneuploidy which causes cancer, and other diseases. Themain criteria for this is the correct duplication of the centrosome. Recently,we reported that Smy2 can suppress the essential role of MPS2 in the insertion of yeast centrosome into the nuclear membraneand co-operates with Eap1, Scp160, Asc1 for this task. We gave the name SESA (Smy2,Eap1, Scp160, Asc1) network to the system consisting ofthese four proteins. Detailed analysis showed that the SESA system is part of amechanism which regulates translation of POM34mRNA. Thus, SESA, is a system which suppresses spindle pole body (SPB)duplication defects by inhibiting the translation of POM34 mRNA (Sezen,et al., 2009). Although many important points regarding SESA networkhave been discovered, many others remain obscure. In this study, we performed agenome-wide screen in order to unearth new members of the system and showedthat Dhh1 is a member of the SESA network. Dhh1 is a known cytoplasmic DEAD-boxhelicase known to play role in translational regulation. Thus we propose thatDhh1 contributes to the highly selective nature of the inhibition of translationby SESA system.