CFDA-SE Finally we find that in the absence of Aurora B

Finally, we find that in the absence of Aurora B, Sgo1 is delocalized from centromeres and found along chromosome arms, as reported after depletion of Bub1 (Kitajima et al., 2005, Riedel et al., 2006). The increased arm cohesion observed in the absence of Aurora B activity is dependent on the presence of Sgo1 (McGuinness et al., 2005; this study). Previously, it has been difficult to understand why chromosome arm cohesion should depend on a centromeric protein such as Sgo1. We suggest that one function of the chromosome passenger complex containing Aurora B is to correctly localize Sgo1 to the centromere, and that the failure of cohesin release after inhibition or depletion of Aurora B (Gimenez-Abian et al., 2004, Losada et al., 2002, McGuinness et al., 2005) may be due in large part to protection of chromosome arm cohesin by ectopic Sgo1 (Figure 4E). Loss of Sgo1 from centromeres in these circumstances, and a resulting loosening of centromeric cohesion, may also explain why primary constrictions are lost after inhibition of Aurora B (Figure 4E) (Gimenez-Abian et al., 2004). In some studies, but not all, Aurora B inactivation decreases Bub1 levels at kinetochores (Ditchfield et al., 2003, Hauf et al., 2003, Meraldi and Sorger, 2005), so one possibility is that Aurora B acts via Bub1 to localize Sgo1. Alternatively, Sgo1 may be phosphorylated by Aurora B or regulated by association with INCENP (Resnick et al., 2006). It is clear that additional study of the mechanisms by which Haspin, Sgo1, Aurora B, and other proteins cooperate to regulate sister CFDA-SE cohesion during mitosis will provide further insight into this complex and critical system.
Experimental Procedures
Acknowledgments
Results
Discussion
Acknowledgments
Introduction Postnatal development of the mouse seminiferous epithelium is a complex process finally produce functional spermatozoa. The whole process can be subdivided into three parts: (i) A premeiotic phase characterized by an increase in cell number due to mitotic divisions of diploid spermatogonia; (ii) a meiotic phase in which pairing and recombination of homologous chromosomes take place to induce genetic variabilities of gametes and to lead to the formation of haploid round spermatids; and (iii) a post meiotic phase, which includes the morphogenetic events required for spermatozoa formation (spermiogenesis) (Russell et al., 1990). The spermatogonial stem cells in the seminiferous epithelium of the adult testis undergo these processes continuously to provide the mature sperms. The precise regulation of germ cell differentiation requires a strict program of stage- and cell-specific gene expressions in germ cells as well as in surrounding somatic cell types (Wolgemuth and Watrin, 1991). To understand the mechanism of testicular germ cell differentiation, it is of great interest to isolate genes specifically expressed in germ cells and to characterize their functions as well as their regulations. We have isolated a lot of cDNAs using a subtraction cloning method (Tanaka et al., 1994). One of them, Gsg3/testicular actin capping-protein has shown to be a unique member of actin capping-proteins. Haspin is another one of them and expressed only in haploid germ cells. The entire coding region of haspin includes just three kinase consensus domains (kinase catalytic domains I to III instead of 12 subdomains) having a Ser/Thr-kinase activity. The protein was exclusively expressed in haploid germ cells of the mouse testis, localized to their nuclei and was able to bind to the DNA. Ectopic expression of Haspin in cultured cells caused cell cycle arrest at G1, resulting in growth arrest of the transfected cells (Tanaka et al., 1999). To elucidate the haspin gene structure and the regulation of gene expression, we isolated haspin genome from mouse (129/Sv strain) genomic library. It existed as an intronless gene in an intron of the gene encoding integrin αM290. As a result, we found a part of a surprising complex genomic structure on mouse chromosome11 (Matsui et al., 1997).