Chromosome alignment on the mitotic spindle is monitored by the spindle checkpoint. We identify Sgo1, a protein involved in meiotic chromosome cohesion, as a spindle checkpoint component. Budding yeast cells with mutations in SGO1 respond normally to microtubule depolymerization but not to lack of tension at the kinetochore, and they have difficulty attaching sister chromatids to opposite poles of the spindle. Sgo1 is thus required for sensing tension between sister chromatids during mitosis, and its degradation when they separate may prevent cell cycle arrest and chromosome loss in anaphase, a time when sister chromatids are no longer under tension.

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The spindle checkpoint delays the onset of anaphase until all pairs of sister chromatids are attached to the mitotic spindle. The checkpoint could monitor the attachment of microtubules to kinetochores, the tension that results from the two sister chromatids attaching to opposite spindle poles, or both. We tested the role of tension by allowing cells to enter mitosis without a prior round of DNA replication. The unreplicated chromatids are attached to spindle microtubules but are not under tension since they lack a sister chromatid that could attach to the opposite pole. Because the spindle checkpoint is activated in these cells, we conclude that the absence of tension at the yeast kinetochore is sufficient to activate the spindle checkpoint in mitosis.

In this article we consider the role of the cyclin-dependent protein kinase cdc2 in regulating progression through the fission yeast cell cycle. The onset of mitosis is governed by cdc2 in partnership with the B-type cyclin, cdc13. Recent evidence shows that the cdc2-cdc13 complex can also control the onset of S phase and, in addition, ensures that there is only one S phase per cell cycle. This leads us to propose a novel quantitative model in which different levels of cdc2 activity regulate cell-cycle progression: S phase is initiated when protein kinase activity increases from a very low to a moderate level; maintenance of this moderate level prevents re-initiation of S phase, and a further increase of activity to a high level initiates mitosis. Inactivation of the kinase activity at the end of mitosis resets the cell for a new cell cycle.

It is critical to elucidate the pathways that mediate spindle assembly and therefore ensure accurate chromosome segregation during cell division. Our studies of a unique allele of the budding yeast Ipl1/Aurora protein kinase revealed that it is required for centrosome-mediated spindle assembly in the absence of the BimC motor protein Cin8. In addition, we found that the Ase1 spindle midzone-associated protein is required for bipolar spindle assembly. The cin8 ipl1 and cin8 ase1 double mutant cells exhibit similar defects, and Ase1 overexpression completely restores spindle assembly in cin8 ipl1 strains. Consistent with the possibility that Ipl1 regulates Ase1, an ase1 mutant lacking the Ipl1 consensus phosphorylation sites cannot assemble spindles in the absence of Cin8. In addition, Ase1 phosphorylation and localization were altered in an ipl1 mutant. We therefore propose that Ipl1/Aurora and Ase1 constitute a previously unidentified spindle assembly pathway that becomes essential in the absence of Cin8.

of this CDK blocks cell cycle progression. The CLN-CDC28 kinase activity promotes the onset of S-phase in Yeast pheromones block cell cycle progression in G 1 two ways (Dirick et al., 1995): it activates the G 1 -specific in order to prepare mating partners for conjugatranscription factors necessary to transcribe genes required tion. We have investigated the mechanism underlying for S-phase (Cross and Tinkelenberg, 1991; Nasmyth and pheromone-induced G 1 arrest in the fission yeast Dirick, 1991) and it inactivates SIC1, an inhibitor of the Schizosaccharomyces pombe. We find that the G 1 -cyclin B-associated CDC28 kinase which is required for specific transcription factor p65 cdc10 -p72 res1/sct1 which the initiation of S-phase (Mendenhall, 1993; Schwob controls the expression of S-phase genes is fully et al., 1994). Given that SIC1 is not essential for the activated in pheromone, unlike the analogous control pheromone response (Nugroho and Mendenhall, 1994), it in budding yeast. In contrast, the G 1 function of p34 cdc2 is the inhibition of the G 1 -specific transcription which is acting after activation of the G 1 -specific transcription the crucial target for the pheromone-induced G 1 arrest in is blocked. Pheromone inhibits the p34 cdc2 kinase budding yeast. associated with both the G 1 -specific B-type cyclinThe mechanism of G 1 arrest in fission yeast is much p45 cig2 and the B-type cyclin p56 cdc13 and overexpresless well understood. Normally the sexual pheromones sion of p45 cig2 or p47 cdc13Δ90 overcomes the pheromone-P-and M-factor only have an effect on nitrogen-starved induced G 1 arrest. G 1 arrest is compromised in enlarged fission yeast cells, because components of the pheromone cells. We suggest that onset of S-phase is controlled by signal transduction cascade are only expressed when pheromone inhibiting the B-cyclin-associated kinase in nutrients are limiting (reviewed in Nielsen and Davey,

Science advances through rich, scholarly discussion. More than ever before, digital tools allow us to take that dialogue online. To chart a new future for open publishing, we must consider alternatives to the core features of the legacy print publishing system, such as an access paywall and editorial selection before publication. Although journals have their strengths, the traditional approach of selecting articles before publication (“curate first, publish second”) forces a focus on “getting into the right journals,” which can delay dissemination of scientific work, create opportunity costs for pushing science forward, and promote undesirable behaviors among scientists and the institutions that evaluate them. We believe that a “publish first, curate second” approach with the following features would be a strong alternative: authors decide when and what to publish; peer review reports are published, either anonymously or with attribution; and curation occurs after publication, incorporating community feedback and expert judgment to select articles for target audiences and to evaluate whether scientific work has stood the test of time. These proposed changes could optimize publishing practices for the digital age, emphasizing transparency, peer-mediated improvement, and post-publication appraisal of scientific articles.

OBITUARY Burton Richter, charm-quark Nobel laureate, remembered p.554 PUBLISHING Preprints-what is good for science is good for the public p.553 Publish peer reviews Jessica K. Polka and colleagues call on journals to sign a pledge to make reviewers' anonymous comments part of the official scientific record.