Recommendations for accelerating open preprint peer review to improve the culture of science.

Peer review is an important part of the scientific process, but traditional peer review at journals is coming under increased scrutiny for its inefficiency and lack of transparency. As preprints become more widely used and accepted, they raise the possibility of rethinking the peer-review process. Preprints are enabling new forms of peer review that have the potential to be more thorough, inclusive, and collegial than traditional journal peer review, and to thus fundamentally shift the culture of peer review toward constructive collaboration. In this Consensus View, we make a call to action to stakeholders in the community to accelerate the growing momentum of preprint sharing and provide recommendations to empower researchers to provide open and constructive peer review for preprints.

A proposal for the future of scientific publishing in the life sciences.

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.

A pathway containing the Ipl1/aurora protein kinase and the spindle midzone protein Ase1 regulates yeast spindle assembly.

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.

Mitosis: aurora gives chromosomes a healthy stretch.

Attachment of sister chromatids to microtubules from opposite spindle poles--bi-orientation--generates tension at the kinetochores. The Ipl1/Aurora B kinase responds to the absence of tension at mono-oriented chromosomes and promotes microtubule turnover and spindle checkpoint activation until a stable bi-oriented attachment is achieved.

The centromeric protein Sgo1 is required to sense lack of tension on mitotic chromosomes.

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.

FEARless in meiosis.

Degradation of mitotic cyclins is critical for exit from mitosis. Recent studies in budding yeast address the role of cyclin degradation in meiosis. Cyclin stabilization in meiosis I interferes with anaphase I spindle disassembly but, surprisingly, does not halt progression into meiosis II.