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            "publicationTitle": "PLoS biology",
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            "date": "Jun 25, 2019",
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            "title": "Disentangling strictly self-serving mutations from win-win mutations in a mutualistic microbial community",
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                    "creatorType": "author",
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                    "lastName": "Hart"
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                    "creatorType": "author",
                    "firstName": "Jose Mario Bello",
                    "lastName": "Pineda"
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            "title": "Spatial self-organization favors heterotypic cooperation over cheating",
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                {
                    "creatorType": "author",
                    "firstName": "Babak",
                    "lastName": "Momeni"
                },
                {
                    "creatorType": "author",
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            "abstractNote": "Cooperation between individuals of the same species, and also between different species, is known to be important in evolution. Large fish, for example, rely on small cleaner fish to remove parasites, while the small fish benefit from the nutrients in these parasites. However, cooperation can be undermined by other individuals or species who “cheat” by taking advantage of those who cooperate, without providing any benefits in return. For example, some cleaner fish cheat by biting off healthy tissue from their host, in addition to parasites.\n\nGenetically-related individuals who cooperate by sharing identical benefits can combat cheaters by giving preferential treatment to their relatives (a process known as kin discrimination) or by staying close to the relatives to form clusters (kin fidelity). However, two genetically-unrelated populations that mutually cooperate by sharing different benefits cannot employ these methods to overcome cheaters. Instead they rely on either partner choice or partner fidelity feedback.\n\nPartner choice – the approach adopted by cleaner fish and their hosts – relies on one population recognizing a signal from the other population and responding accordingly: for example, large fish observe cleaner fish and approach those that cooperate with their current host and avoid those that cheat. Partner fidelity feedback, on the other hand, relies on repeated interactions between the two populations providing an advantage in terms of evolutionary fitness to both: for example, organelles called mitochondria and chloroplasts live inside cells, helping the cells to harvest energy and providing energy for themselves and the host cells in the process. In some cases – such as the cooperation between figs and fig wasps, or between certain plants and the bacteria that fix nitrogen in their roots – researchers cannot agree if the populations are relying on partner choice or partner fidelity feedback.\n\nNow Momeni et al. have used a combination of experiments on yeast and mathematical modeling to explore partner fidelity feedback in greater detail. They started by using genetic engineering techniques to produce two species of yeast that mutually cooperate, each providing a metabolite that is essential to the other, but are not able to recognize each other: this means that these populations cannot rely on partner choice to combat cheaters. Momeni et al. then observed how these two species interacted with each other and a third species of yeast that cheated by consuming one of the metabolites without releasing any metabolite of its own . \n\nMomeni et al. found that as long as there was space for the yeast cells to grow into, the two species that cooperated self-organized into mixed clusters, with the cheating species being excluded from these clusters. The self-organization was driven by a positive feedback loop involving the two species that cooperated, with each species helping to increase the fitness of the other. The results of Momeni et al. demonstrate that it is possible for two genetically unrelated populations to cooperate and combat cheaters without the use of partner choice.\n\nDOI: [http://dx.doi.org/10.7554/eLife.00960.002][1]\n\n [1]: /lookup/doi/10.7554/eLife.00960.002",
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            "rights": "Copyright © 2013, Momeni et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.",
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                    "tag": "S. cerevisiae",
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                    "creatorType": "author",
                    "firstName": "Wenying",
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                    "creatorType": "author",
                    "firstName": "Ramzi",
                    "lastName": "Azzam"
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                    "creatorType": "author",
                    "firstName": "Susan L",
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                    "creatorType": "author",
                    "firstName": "Roland S",
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                {
                    "creatorType": "author",
                    "firstName": "Steve A",
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                {
                    "creatorType": "author",
                    "firstName": "Raymond J",
                    "lastName": "Deshaies"
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            ],
            "abstractNote": "BACKGROUND\n\nIn S. cerevisiae, the mitotic exit network (MEN) proteins, including the Polo-like protein kinase Cdc5 and the protein phosphatase Cdc14, are required for exit from mitosis. In pre-anaphase cells, Cdc14 is sequestered to the nucleolus by Net1 as a part of the RENT complex. When cells are primed to exit mitosis, the RENT complex is disassembled and Cdc14 is released from the nucleolus.\n\n\nRESULTS\n\nHere, we show that Cdc5 is necessary to free nucleolar Cdc14 in late mitosis, that elevated Cdc5 activity provokes ectopic release of Cdc14 in pre-anaphase cells, and that the phosphorylation state of Net1 is regulated by Cdc5 during anaphase. Furthermore, recombinant Cdc5 and Xenopus Polo-like kinase can disassemble the RENT complex in vitro by phosphorylating Net1 and thereby reducing its affinity for Cdc14. Surprisingly, although RENT complexes containing Net1 mutants (Net1(7m) and Net1(19m') lacking sites phosphorylated by Cdc5 in vitro are refractory to disassembly by Polo-like kinases in vitro, net1(7m) and net1(19m') cells grow normally and exhibit only minor defects in releasing Cdc14 during anaphase. However, net1(19m') cells exhibit a synergistic growth defect when combined with mutations in CDC5 or DBF2 (another MEN gene).\n\n\nCONCLUSIONS\n\nWe propose that although Cdc5 potentially disassembles RENT by directly phosphorylating Net1, Cdc5 mediates exit from mitosis primarily by phosphorylating other targets. Our study suggests that Cdc5/Polo is unusually promiscuous and highlights the need to validate Cdc5/Polo in vitro phosphorylation sites by direct in vivo mapping experiments.",
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            "websiteTitle": "",
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            "tags": [
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                    "tag": "Clinical Laboratory Techniques",
                    "type": 1
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                {
                    "tag": "Cytological Techniques",
                    "type": 1
                },
                {
                    "tag": "Investigative Techniques",
                    "type": 1
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                    "tag": "Life Sciences (General)",
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                    "creatorType": "author",
                    "firstName": "Babak",
                    "lastName": "Momeni"
                },
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                    "creatorType": "author",
                    "firstName": "Chi-Chun",
                    "lastName": "Chen"
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                    "creatorType": "author",
                    "firstName": "Kristina L",
                    "lastName": "Hillesland"
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            "abstractNote": "The web of life is weaved from diverse symbiotic interactions between species. Symbioses vary from antagonistic interactions such as competition and predation to beneficial interactions such as mutualism. What are the bases for the origin and persistence of symbiosis? What affects the ecology and evolution of symbioses? How do symbiotic interactions generate ecological patterns? How do symbiotic partners evolve and coevolve? Many of these questions are difficult to address in natural systems. Artificial systems, from abstract to living, have been constructed to capture essential features of natural symbioses and to address these key questions. With reduced complexity and increased controllability, artificial systems can serve as useful models for natural systems. We review how artificial systems have contributed to our understanding of symbioses.",
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                    "firstName": "A F",
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                    "creatorType": "author",
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                    "firstName": "D",
                    "lastName": "Moazed"
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            "abstractNote": "The Sir2 protein mediates gene silencing and repression of recombination at the rDNA repeats in budding yeast. Here we show that Sir2 executes these functions as a component of a nucleolar complex designated RENT (regulator of nucleolar silencing and telophase exit). Net1, a core subunit of this complex, preferentially cross-links to the rDNA repeats, but not to silent DNA regions near telomeres or to active genes, and tethers the RENT complex to rDNA. Net1 is furthermore required for rDNA silencing and nucleolar integrity. During interphase, Net1 and Sir2 colocalize to a subdomain within the nucleous, but at the end of mitosis a fraction of Sir2 leaves the nucleolus and disperses as foci throughout the nucleus, suggesting that the structure of rDNA silent chromatin changes during the cell cycle. Our findings suggest that a protein complex shown to regulate exit from mitosis is also involved in gene silencing.",
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            "volume": "97",
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                    "tag": "DNA, Fungal",
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                },
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                {
                    "tag": "Silent Information Regulator Proteins, Saccharomyces cerevisiae",
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                {
                    "tag": "Sirtuin 2",
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                {
                    "tag": "Sirtuins",
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                    "tag": "Trans-Activators",
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