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Importantly, this severing with the Golgi ribbon is essential for T, 2007). Importantly, this severing in the Golgi ribbon is important for entry into mitosis (Sutterlin et al., 2002; E. Interestingly, members in the CCT have already been implicated in multiplication Hidalgo Carcedo et al., 2004; Colanzi and Corda, 2007; Colanzi et al., 2007; Feinstein and Linstedt, 2007).This short article was published on the net ahead of print in MBoC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E10 030243) on September 15, 2010. Address correspondence to: Antonino Colanzi ([email protected]). Abbreviations employed: AurA, AuroraA; GST, glutathione transferase; SBD, BARS substratebinding domain. 2010 A. Persico et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months right after publication it is out there to the public below an Attribution oncommercial hare Alike 3.0 Unported Inventive Commons License (http://creativecommons.org/licenses/byncsa/3.0).A functional block from the proteins involved in this Golgi fragmentation step, like the fissioning protein CtBP1S/ BARS (henceforth referred to as BARS) (Hidalgo Carcedo et al., 2004; Corda et al., 2006) along with the Golgi matrix components GRASP65 (Sutterlin et al., 2002) and GRASP55 (Duran et al., 2008), benefits in Ithout replenishing with fresh culture medium containing butyrate. Contemplating that butyrate inhibition in the severing in the Golgi ribbon and arrest from the cell cycle in the G2 stage (Sutterlin et al., 2002; Hidalgo Carcedo et al., 2004; Yoshimura et al., 2005). Inhibition or depletion in the kinases that control this Golgi fragmentation, including Raf1, Mek1 and Erk1c, also final results inside a substantial delay in G2/M transition (Acharya et al., 1998; Colanzi et al., 2003; Shaul and Seger, 2006; Feinstein and Linstedt, 2007). Once in mitosis, the Golgi stacks undergo additional fragmentation, that is independent of BARS (Colanzi et al., 2007) and Mek1 (Feinstein and Linstedt, 2007) and is controlled by Cdk1 and Pololike kinase1 (Plk1) (Wang et al., 2005; Colanzi and Corda, 2007). Thus, a "Golgi mitotic checkpoint" is dedicated to linking the state of (dis)assembly from the Golgi complicated with entry into mitosis (Colanzi and Corda, 2007; Rabouille and Kondylis, 2007). The molecular mechanisms connecting Golgi fragmentation to regulation of mitotic progression are nevertheless not known, and their elucidation has the potential for identification of novel proteins/mechanisms which can be involved within the overall maintenance on the structure and function in the Golgi complicated and in cell cycle regulation. Here, we show that severing with the Golgi ribbon through G2 is concomitant to centrosome separation and to centrosome recruitment and activation of your mitotic kinase AuroraA (AurA), an essential regulator of entry into mitosis (Hirota et al., 2003; Seki et al., 2008). To identify the cell cycle proteins which can be targeted by the Golgi checkpoint, we induced an acute block of Golgi partitioning in cells synchronized for mitotic ingression and analyzed the functional consequences of this inhibition of Golgi fragmentation. We come across that a block in Golgi partitioning induces sturdy imAuroraA Regulation by Golgi Partitioningpairment of recruitment and activation of AurA at the centrosome, and this results in a block of cell entry into mitosis. Overexpression of AurA can overcome the cell cycle block induced by inhibition of Golgi fragmentation, indicating that this kinase is often a important effector of this Golgi checkpoint.