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Abstract Meiosis in the budding yeast Saccharomyces cerevisiae is used to create haploid yeast spores from a diploid mother cell. During meiosis II, cytokinesis occurs by closure of the prospore membrane, a membrane that initiates at the spindle pole body and grows to surround each of the haploid meiotic products. Timely prospore membrane closure requires SPS1, which encodes an STE20 family GCKIII kinase. To identify genes that may activate SPS1, we utilized a histone phosphorylation defect of sps1 mutants to screen for genes with a similar phenotype and found that cdc15 shared this phenotype. CDC15 encodes a Hippo-like kinase that is part of the mitotic exit network. We find that Sps1 complexes with Cdc15, that Sps1 phosphorylation requires Cdc15, and that CDC15 is also required for timely prospore membrane closure. We also find that SPS1, like CDC15, is required for meiosis II spindle disassembly and sustained anaphase II release of Cdc14 in meiosis. However, the NDR-kinase complex encoded by DBF2/DBF20MOB1 which functions downstream of CDC15 in mitotic cells, does not appear to play a role in spindle disassembly, timely prospore membrane closure, or sustained anaphase II Cdc14 release. Taken together, our results suggest that the mitotic exit network is rewired for exit from meiosis II, such that SPS1 replaces the NDR-kinase complex downstream of CDC15. 

During sporulation in the budding yeast Saccharomyces cerevisiae, proper development of the prospore membrane is necessary for the formation of viable spores. The prospore membrane will eventually become the plasma membrane of the newly formed haploid spore and also serves as the template for the deposition of the spore wall. The prospore membrane is generated de novo during meiosis II and the growing edge of the prospore membrane is associated with the Leading Edge Protein (LEP) complex. We find that the Smk1 MAP kinase, along with its activator Ssp2, transiently localizes with the LEP during late meiosis II. SSP2 is required for the leading edge localization of Smk1; this localization is independent of the activation state of Smk1. Like other LEP components, the localization of Smk1 at the leading edge also depends on Ady3. Although prospore membrane development begins normally in smk1 and ssp2 mutants, late prospore membrane formation is disrupted, with the formation of ectopic membrane compartments. Thus, MAP kinase signaling plays an important role in the formation of the prospore membrane. 

Abstract Anolis lizards are well known for their specialist ecomorphs characterized by the convergent evolution of suites of traits linked to the use of particular microhabitats. Many of these same traits evolve rapidly in response to novel selection pressures and have been very well studied. In contrast, the tail crest, a feature present in a subset of lineages, has been almost entirely overlooked. Variation in tail crest morphology within and among species remains largely unstudied, as does the function of the trait. Here, we use the natural experiment provided by urbanization to ask whether tail crest size differs between urban and forest populations of the crested anole (Anolis cristatellus) across the Caribbean island of Puerto Rico. We find that tail crest size differs primarily between regions; however, within regions, crests are invariably larger in urban than in forest environments. This difference in size is correlated with the hotter, drier conditions and sparser distribution of perches that typify urban sites, leading to the intriguing possibility that the tail crest might be under differential natural selection for signalling and/or because of the thermoregulatory challenge of urban habitats. Further study is required to shed light on the functional significance and evolution of this under-studied trait.