Aki1 helps centrioles stay tight

Aki1 helps centrioles stay tight D uplicated centrioles are codependent, remaining attached until the end of mitosis. An unlikely protein helps hold the structures together by enlisting one of the tethers that connects sister chromatids, Nakamura et al. show. Replicated pairs of centrioles relocate to opposite ends of a dividing cell, but the members of each pair remain linked until the end of mitosis. Researchers are starting to unravel how cells control this connection and have already found overlap with the mechanisms that join and part sister chromatids. Centri-oles harbor some members of the cohesin complex that lashes chromatids together. The enzyme separase, which cleaves sister chromatids, also splits up centriole pairs. Nakamura et al. discovered that centrosomes harbor the protein Aki1, which is involved in epidermal growth factor signaling. But when they investigated further, the team found that Aki1 also promotes centriole togetherness. In cells lacking the protein, centri-ole pairs divorce prematurely, resulting in multipolar spindles. These cells trip the spindle checkpoint and eventually commit suicide. The cohesin component Scc1 prevents centrioles from splitting too soon, the researchers showed. Aki1 sticks to Scc1 and another cohesin component, SA-2. The results suggest that Aki1 helps direct Scc1 to the centrosome, where it can fasten centri-oles together. The next step, the researchers say, is determining why Aki1 helps connect centrioles but not sister chromatids. G uan et al. suggest a function for mysterious DNA segments that are scattered throughout the mammalian genome. The segments curtail most or all replication within their boundaries and might allow cells to fine-tune the pace of DNA duplication. Different parts of the genome replicate at different times in S phase. Some sections start the process early, whereas others procrastinate. A third category contains the temporal transition regions, or TTRs, that start replicating at the beginning of S phase but don't fi nish until late. How cells control the timing of TTR duplication is unknown. A possible clue comes from the gene locus for the antibody heavy chain. In embryonic stem cells, these genes are located within a TTR. But early in B cell development, the TTR appears to vanish, and the entire locus replicates early. This indicates that the TTR harbors latent replication origins that can be turned on. Guan et al. wanted to discover how. Genes that are being transcribed typically duplicate before inactive ones. To test whether transcription affects TTR replica-tion, Guan et al. …