Pub Date : 2024-09-12DOI: 10.1371/journal.pbio.3002809
Peter S. Back, Vignesh Senthilkumar, Charles P. Choi, Justin J. Quan, Qing Lou, Anne K. Snyder, Andrew M. Ly, Justin G. Lau, Z. Hong Zhou, Gary E. Ward, Peter J. Bradley
Apicomplexan parasites possess several specialized structures to invade their host cells and replicate successfully. One of these is the inner membrane complex (IMC), a peripheral membrane-cytoskeletal system underneath the plasma membrane. It is composed of a series of flattened, membrane-bound vesicles and a cytoskeletal subpellicular network (SPN) comprised of intermediate filament-like proteins called alveolins. While the alveolin proteins are conserved throughout the Apicomplexa and the broader Alveolata, their precise functions and interactions remain poorly understood. Here, we describe the function of one of these alveolin proteins in Toxoplasma, IMC6. Disruption of IMC6 resulted in striking morphological defects that led to aberrant invasion and replication but surprisingly minor effects on motility. Deletion analyses revealed that the alveolin domain alone is largely sufficient to restore localization and partially sufficient for function. As this highlights the importance of the IMC6 alveolin domain, we implemented unnatural amino acid photoreactive crosslinking to the alveolin domain and identified multiple binding interfaces between IMC6 and 2 other cytoskeletal IMC proteins—IMC3 and ILP1. This provides direct evidence of protein–protein interactions in the alveolin domain and supports the long-held hypothesis that the alveolin domain is responsible for filament formation. Collectively, our study features the conserved alveolin proteins as critical components that maintain the parasite’s structural integrity and highlights the alveolin domain as a key mediator of SPN architecture.
{"title":"Alveolin proteins in the Toxoplasma inner membrane complex form a highly interconnected structure that maintains parasite shape and replication","authors":"Peter S. Back, Vignesh Senthilkumar, Charles P. Choi, Justin J. Quan, Qing Lou, Anne K. Snyder, Andrew M. Ly, Justin G. Lau, Z. Hong Zhou, Gary E. Ward, Peter J. Bradley","doi":"10.1371/journal.pbio.3002809","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002809","url":null,"abstract":"Apicomplexan parasites possess several specialized structures to invade their host cells and replicate successfully. One of these is the inner membrane complex (IMC), a peripheral membrane-cytoskeletal system underneath the plasma membrane. It is composed of a series of flattened, membrane-bound vesicles and a cytoskeletal subpellicular network (SPN) comprised of intermediate filament-like proteins called alveolins. While the alveolin proteins are conserved throughout the Apicomplexa and the broader Alveolata, their precise functions and interactions remain poorly understood. Here, we describe the function of one of these alveolin proteins in <jats:italic>Toxoplasma</jats:italic>, IMC6. Disruption of IMC6 resulted in striking morphological defects that led to aberrant invasion and replication but surprisingly minor effects on motility. Deletion analyses revealed that the alveolin domain alone is largely sufficient to restore localization and partially sufficient for function. As this highlights the importance of the IMC6 alveolin domain, we implemented unnatural amino acid photoreactive crosslinking to the alveolin domain and identified multiple binding interfaces between IMC6 and 2 other cytoskeletal IMC proteins—IMC3 and ILP1. This provides direct evidence of protein–protein interactions in the alveolin domain and supports the long-held hypothesis that the alveolin domain is responsible for filament formation. Collectively, our study features the conserved alveolin proteins as critical components that maintain the parasite’s structural integrity and highlights the alveolin domain as a key mediator of SPN architecture.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-11DOI: 10.1371/journal.pbio.3002784
Wen Wen, Shrey Grover, Douglas Hazel, Peyton Berning, Frederik Baumgardt, Vighnesh Viswanathan, Olivia Tween, Robert M. G. Reinhart
Maintaining and removing information in mind are 2 fundamental cognitive processes that decline sharply with age. Using a combination of beta-band neural oscillations, which have been implicated in the regulation of working memory contents, and cross-trial neural variability, an undervalued property of brain dynamics theorized to govern adaptive cognitive processes, we demonstrate an age-related dissociation between distinct working memory functions—information maintenance and post-response deletion. Load-dependent decreases in beta variability during maintenance predicted memory performance of younger, but not older adults. Surprisingly, the post-response phase emerged as the predictive locus of working memory performance for older adults, with post-response beta variability correlated with memory performance of older, but not younger adults. Single-trial analysis identified post-response beta power elevation as a frequency-specific signature indexing memory deletion. Our findings demonstrate the nuanced interplay between age, beta dynamics, and working memory, offering valuable insights into the neural mechanisms of cognitive decline in agreement with the inhibition deficit theory of aging.
{"title":"Beta-band neural variability reveals age-related dissociations in human working memory maintenance and deletion","authors":"Wen Wen, Shrey Grover, Douglas Hazel, Peyton Berning, Frederik Baumgardt, Vighnesh Viswanathan, Olivia Tween, Robert M. G. Reinhart","doi":"10.1371/journal.pbio.3002784","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002784","url":null,"abstract":"Maintaining and removing information in mind are 2 fundamental cognitive processes that decline sharply with age. Using a combination of beta-band neural oscillations, which have been implicated in the regulation of working memory contents, and cross-trial neural variability, an undervalued property of brain dynamics theorized to govern adaptive cognitive processes, we demonstrate an age-related dissociation between distinct working memory functions—information maintenance and post-response deletion. Load-dependent decreases in beta variability during maintenance predicted memory performance of younger, but not older adults. Surprisingly, the post-response phase emerged as the predictive locus of working memory performance for older adults, with post-response beta variability correlated with memory performance of older, but not younger adults. Single-trial analysis identified post-response beta power elevation as a frequency-specific signature indexing memory deletion. Our findings demonstrate the nuanced interplay between age, beta dynamics, and working memory, offering valuable insights into the neural mechanisms of cognitive decline in agreement with the inhibition deficit theory of aging.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1371/journal.pbio.3002790
Tim Rohe, Klaus Hesse, Ann-Christine Ehlis, Uta Noppeney
Hallucinations and perceptual abnormalities in psychosis are thought to arise from imbalanced integration of prior information and sensory inputs. We combined psychophysics, Bayesian modeling, and electroencephalography (EEG) to investigate potential changes in perceptual and causal inference in response to audiovisual flash-beep sequences in medicated individuals with schizophrenia who exhibited limited psychotic symptoms. Seventeen participants with schizophrenia and 23 healthy controls reported either the number of flashes or the number of beeps of audiovisual sequences that varied in their audiovisual numeric disparity across trials. Both groups balanced sensory integration and segregation in line with Bayesian causal inference rather than resorting to simpler heuristics. Both also showed comparable weighting of prior information regarding the signals’ causal structure, although the schizophrenia group slightly overweighted prior information about the number of flashes or beeps. At the neural level, both groups computed Bayesian causal inference through dynamic encoding of independent estimates of the flash and beep counts, followed by estimates that flexibly combine audiovisual inputs. Our results demonstrate that the core neurocomputational mechanisms for audiovisual perceptual and causal inference in number estimation tasks are largely preserved in our limited sample of medicated post-acute individuals with schizophrenia. Future research should explore whether these findings generalize to unmedicated patients with acute psychotic symptoms.
{"title":"Multisensory perceptual and causal inference is largely preserved in medicated post-acute individuals with schizophrenia","authors":"Tim Rohe, Klaus Hesse, Ann-Christine Ehlis, Uta Noppeney","doi":"10.1371/journal.pbio.3002790","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002790","url":null,"abstract":"Hallucinations and perceptual abnormalities in psychosis are thought to arise from imbalanced integration of prior information and sensory inputs. We combined psychophysics, Bayesian modeling, and electroencephalography (EEG) to investigate potential changes in perceptual and causal inference in response to audiovisual flash-beep sequences in medicated individuals with schizophrenia who exhibited limited psychotic symptoms. Seventeen participants with schizophrenia and 23 healthy controls reported either the number of flashes or the number of beeps of audiovisual sequences that varied in their audiovisual numeric disparity across trials. Both groups balanced sensory integration and segregation in line with Bayesian causal inference rather than resorting to simpler heuristics. Both also showed comparable weighting of prior information regarding the signals’ causal structure, although the schizophrenia group slightly overweighted prior information about the number of flashes or beeps. At the neural level, both groups computed Bayesian causal inference through dynamic encoding of independent estimates of the flash and beep counts, followed by estimates that flexibly combine audiovisual inputs. Our results demonstrate that the core neurocomputational mechanisms for audiovisual perceptual and causal inference in number estimation tasks are largely preserved in our limited sample of medicated post-acute individuals with schizophrenia. Future research should explore whether these findings generalize to unmedicated patients with acute psychotic symptoms.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1371/journal.pbio.3002815
Richard J. Abdill, Emma Talarico, Laura Grieneisen
In 2024, all biology is computational biology. Computer-aided analysis continues to spread into new fields, becoming more accessible to researchers trained in the wet lab who are eager to take advantage of growing datasets, falling costs, and novel assays that present new opportunities for discovery. It is currently much easier to find guidance for implementing these techniques than for reporting their use, leaving biologists to guess which details and files are relevant. In this essay, we review existing literature on the topic, summarize common tips, and link to additional resources for training. Following this overview, we then provide a set of recommendations for sharing code, with an eye toward guiding those who are comparatively new to applying open science principles to their computational work. Taken together, we provide a guide for biologists who seek to follow code sharing best practices but are unsure where to start.
{"title":"A how-to guide for code sharing in biology","authors":"Richard J. Abdill, Emma Talarico, Laura Grieneisen","doi":"10.1371/journal.pbio.3002815","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002815","url":null,"abstract":"In 2024, all biology is computational biology. Computer-aided analysis continues to spread into new fields, becoming more accessible to researchers trained in the wet lab who are eager to take advantage of growing datasets, falling costs, and novel assays that present new opportunities for discovery. It is currently much easier to find guidance for implementing these techniques than for reporting their use, leaving biologists to guess which details and files are relevant. In this essay, we review existing literature on the topic, summarize common tips, and link to additional resources for training. Following this overview, we then provide a set of recommendations for sharing code, with an eye toward guiding those who are comparatively new to applying open science principles to their computational work. Taken together, we provide a guide for biologists who seek to follow code sharing best practices but are unsure where to start.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1371/journal.pbio.3002791
Asma Sarah Khelifa, Maanasa Bhaskaran, Tom Boissavy, Thomas Mouveaux, Tatiana Araujo Silva, Cerina Chhuon, Marcia Attias, Ida Chiara Guerrera, Wanderley De Souza, David Dauvillee, Emmanuel Roger, Mathieu Gissot
Virulence of apicomplexan parasites is based on their ability to divide rapidly to produce significant biomass. The regulation of their cell cycle is therefore key to their pathogenesis. Phosphorylation is a crucial posttranslational modification that regulates many aspects of the eukaryotic cell cycle. The phosphatase PP1 is known to play a major role in the phosphorylation balance in eukaryotes. We explored the role of TgPP1 during the cell cycle of the tachyzoite form of the apicomplexan parasite Toxoplasma gondii. Using a conditional mutant strain, we show that TgPP1 regulates many aspects of the cell cycle including the proper assembly of the daughter cells’ inner membrane complex (IMC), the segregation of organelles, and nuclear division. Unexpectedly, depletion of TgPP1 also results in the accumulation of amylopectin, a storage polysaccharide that is usually found in the latent bradyzoite form of the parasite. Using transcriptomics and phospho-proteomics, we show that TgPP1 mainly acts through posttranslational mechanisms by dephosphorylating target proteins including IMC proteins. TgPP1 also dephosphorylates a protein bearing a starch-binding domain. Mutagenesis analysis reveals that the targeted phospho-sites are linked to the ability of the parasite to regulate amylopectin steady-state levels. Therefore, we show that TgPP1 has pleiotropic roles during the tachyzoite cell cycle regulation, but also regulates amylopectin accumulation.
{"title":"PP1 phosphatase controls both daughter cell formation and amylopectin levels in Toxoplasma gondii","authors":"Asma Sarah Khelifa, Maanasa Bhaskaran, Tom Boissavy, Thomas Mouveaux, Tatiana Araujo Silva, Cerina Chhuon, Marcia Attias, Ida Chiara Guerrera, Wanderley De Souza, David Dauvillee, Emmanuel Roger, Mathieu Gissot","doi":"10.1371/journal.pbio.3002791","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002791","url":null,"abstract":"Virulence of apicomplexan parasites is based on their ability to divide rapidly to produce significant biomass. The regulation of their cell cycle is therefore key to their pathogenesis. Phosphorylation is a crucial posttranslational modification that regulates many aspects of the eukaryotic cell cycle. The phosphatase PP1 is known to play a major role in the phosphorylation balance in eukaryotes. We explored the role of TgPP1 during the cell cycle of the tachyzoite form of the apicomplexan parasite <jats:italic>Toxoplasma gondii</jats:italic>. Using a conditional mutant strain, we show that TgPP1 regulates many aspects of the cell cycle including the proper assembly of the daughter cells’ inner membrane complex (IMC), the segregation of organelles, and nuclear division. Unexpectedly, depletion of TgPP1 also results in the accumulation of amylopectin, a storage polysaccharide that is usually found in the latent bradyzoite form of the parasite. Using transcriptomics and phospho-proteomics, we show that TgPP1 mainly acts through posttranslational mechanisms by dephosphorylating target proteins including IMC proteins. TgPP1 also dephosphorylates a protein bearing a starch-binding domain. Mutagenesis analysis reveals that the targeted phospho-sites are linked to the ability of the parasite to regulate amylopectin steady-state levels. Therefore, we show that TgPP1 has pleiotropic roles during the tachyzoite cell cycle regulation, but also regulates amylopectin accumulation.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1371/journal.pbio.3002802
Mohammad Zeeshan, Ravish Rashpa, David J. Ferguson, George Mckeown, Raushan Nugmanova, Amit K. Subudhi, Raphael Beyeler, Sarah L. Pashley, Robert Markus, Declan Brady, Magali Roques, Andrew R. Bottrill, Andrew M. Fry, Arnab Pain, Sue Vaughan, Anthony A. Holder, Eelco C. Tromer, Mathieu Brochet, Rita Tewari
Mitosis is an important process in the cell cycle required for cells to divide. Never in mitosis (NIMA)-like kinases (NEKs) are regulators of mitotic functions in diverse organisms. Plasmodium spp., the causative agent of malaria is a divergent unicellular haploid eukaryote with some unusual features in terms of its mitotic and nuclear division cycle that presumably facilitate proliferation in varied environments. For example, during the sexual stage of male gametogenesis that occurs within the mosquito host, an atypical rapid closed endomitosis is observed. Three rounds of genome replication from 1N to 8N and successive cycles of multiple spindle formation and chromosome segregation occur within 8 min followed by karyokinesis to generate haploid gametes. Our previous Plasmodium berghei kinome screen identified 4 Nek genes, of which 2, NEK2 and NEK4, are required for meiosis. NEK1 is likely to be essential for mitosis in asexual blood stage schizogony in the vertebrate host, but its function during male gametogenesis is unknown. Here, we study NEK1 location and function, using live cell imaging, ultrastructure expansion microscopy (U-ExM), and electron microscopy, together with conditional gene knockdown and proteomic approaches. We report spatiotemporal NEK1 location in real-time, coordinated with microtubule organising centre (MTOC) dynamics during the unusual mitoses at various stages of the Plasmodium spp. life cycle. Knockdown studies reveal NEK1 to be an essential component of the MTOC in male cell differentiation, associated with rapid mitosis, spindle formation, and kinetochore attachment. These data suggest that P. berghei NEK1 kinase is an important component of MTOC organisation and essential regulator of chromosome segregation during male gamete formation.
{"title":"Plasmodium NEK1 coordinates MTOC organisation and kinetochore attachment during rapid mitosis in male gamete formation","authors":"Mohammad Zeeshan, Ravish Rashpa, David J. Ferguson, George Mckeown, Raushan Nugmanova, Amit K. Subudhi, Raphael Beyeler, Sarah L. Pashley, Robert Markus, Declan Brady, Magali Roques, Andrew R. Bottrill, Andrew M. Fry, Arnab Pain, Sue Vaughan, Anthony A. Holder, Eelco C. Tromer, Mathieu Brochet, Rita Tewari","doi":"10.1371/journal.pbio.3002802","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002802","url":null,"abstract":"Mitosis is an important process in the cell cycle required for cells to divide. Never in mitosis (NIMA)-like kinases (NEKs) are regulators of mitotic functions in diverse organisms. <jats:italic>Plasmodium</jats:italic> spp., the causative agent of malaria is a divergent unicellular haploid eukaryote with some unusual features in terms of its mitotic and nuclear division cycle that presumably facilitate proliferation in varied environments. For example, during the sexual stage of male gametogenesis that occurs within the mosquito host, an atypical rapid closed endomitosis is observed. Three rounds of genome replication from 1N to 8N and successive cycles of multiple spindle formation and chromosome segregation occur within 8 min followed by karyokinesis to generate haploid gametes. Our previous <jats:italic>Plasmodium berghei</jats:italic> kinome screen identified 4 <jats:italic>Nek</jats:italic> genes, of which 2, NEK2 and NEK4, are required for meiosis. NEK1 is likely to be essential for mitosis in asexual blood stage schizogony in the vertebrate host, but its function during male gametogenesis is unknown. Here, we study NEK1 location and function, using live cell imaging, ultrastructure expansion microscopy (U-ExM), and electron microscopy, together with conditional gene knockdown and proteomic approaches. We report spatiotemporal NEK1 location in real-time, coordinated with microtubule organising centre (MTOC) dynamics during the unusual mitoses at various stages of the <jats:italic>Plasmodium</jats:italic> spp. life cycle. Knockdown studies reveal NEK1 to be an essential component of the MTOC in male cell differentiation, associated with rapid mitosis, spindle formation, and kinetochore attachment. These data suggest that <jats:italic>P</jats:italic>. <jats:italic>berghei</jats:italic> NEK1 kinase is an important component of MTOC organisation and essential regulator of chromosome segregation during male gamete formation.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1371/journal.pbio.3002755
Lara Urban,Anna W Santure,Lydia Uddstrom,Andrew Digby,Deidre Vercoe,Daryl Eason,Jodie Crane,,Matthew J Wylie,Tāne Davis,Marissa F LeLec,Joseph Guhlin,Simon Poulton,Jon Slate,Alana Alexander,Patricia Fuentes-Cross,Peter K Dearden,Neil J Gemmell,Farhan Azeem,Marvin Weyland,Harald G L Schwefel,Cock van Oosterhout,Hernán E Morales
The information contained in population genomic data can tell us much about the past ecology and evolution of species. We leveraged detailed phenotypic and genomic data of nearly all living kākāpō to understand the evolution of its feather color polymorphism. The kākāpō is an endangered and culturally significant parrot endemic to Aotearoa New Zealand, and the green and olive feather colorations are present at similar frequencies in the population. The presence of such a neatly balanced color polymorphism is remarkable because the entire population currently numbers less than 250 birds, which means it has been exposed to severe genetic drift. We dissected the color phenotype, demonstrating that the two colors differ in their light reflectance patterns due to differential feather structure. We used quantitative genomics methods to identify two genetic variants whose epistatic interaction can fully explain the species' color phenotype. Our genomic forward simulations show that balancing selection might have been pivotal to establish the polymorphism in the ancestrally large population, and to maintain it during population declines that involved a severe bottleneck. We hypothesize that an extinct apex predator was the likely agent of balancing selection, making the color polymorphism in the kākāpō a "ghost of selection past."
{"title":"The genetic basis of the kākāpō structural color polymorphism suggests balancing selection by an extinct apex predator.","authors":"Lara Urban,Anna W Santure,Lydia Uddstrom,Andrew Digby,Deidre Vercoe,Daryl Eason,Jodie Crane,,Matthew J Wylie,Tāne Davis,Marissa F LeLec,Joseph Guhlin,Simon Poulton,Jon Slate,Alana Alexander,Patricia Fuentes-Cross,Peter K Dearden,Neil J Gemmell,Farhan Azeem,Marvin Weyland,Harald G L Schwefel,Cock van Oosterhout,Hernán E Morales","doi":"10.1371/journal.pbio.3002755","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002755","url":null,"abstract":"The information contained in population genomic data can tell us much about the past ecology and evolution of species. We leveraged detailed phenotypic and genomic data of nearly all living kākāpō to understand the evolution of its feather color polymorphism. The kākāpō is an endangered and culturally significant parrot endemic to Aotearoa New Zealand, and the green and olive feather colorations are present at similar frequencies in the population. The presence of such a neatly balanced color polymorphism is remarkable because the entire population currently numbers less than 250 birds, which means it has been exposed to severe genetic drift. We dissected the color phenotype, demonstrating that the two colors differ in their light reflectance patterns due to differential feather structure. We used quantitative genomics methods to identify two genetic variants whose epistatic interaction can fully explain the species' color phenotype. Our genomic forward simulations show that balancing selection might have been pivotal to establish the polymorphism in the ancestrally large population, and to maintain it during population declines that involved a severe bottleneck. We hypothesize that an extinct apex predator was the likely agent of balancing selection, making the color polymorphism in the kākāpō a \"ghost of selection past.\"","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-09DOI: 10.1371/journal.pbio.3002816
Nicholas J. L. Brown
During the last decade, there has been a substantial acceleration in the open science movement. Most people would probably hope to have seen signs of positive change in that time, yet it seems that the process of improving the practice of science is moving at a glacial pace.
{"title":"Fixing science means an end to gaming the system","authors":"Nicholas J. L. Brown","doi":"10.1371/journal.pbio.3002816","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002816","url":null,"abstract":"During the last decade, there has been a substantial acceleration in the open science movement. Most people would probably hope to have seen signs of positive change in that time, yet it seems that the process of improving the practice of science is moving at a glacial pace.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142195502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-15DOI: 10.1371/journal.pbio.3002754
Jaromir Novak, Jiri Neuzil
Horizontal mitochondrial transfer (HMT) has emerged as a novel phenomenon in cell biology, but it is unclear how this process of intercellular movement of mitochondria is regulated. A new study in PLOS Biology reports that ADP released by stressed cells is a signal that triggers HMT.
{"title":"To transfer mitochondria or not to transfer mitochondria: ADP does the trick","authors":"Jaromir Novak, Jiri Neuzil","doi":"10.1371/journal.pbio.3002754","DOIUrl":"https://doi.org/10.1371/journal.pbio.3002754","url":null,"abstract":"Horizontal mitochondrial transfer (HMT) has emerged as a novel phenomenon in cell biology, but it is unclear how this process of intercellular movement of mitochondria is regulated. A new study in <jats:italic>PLOS Biology</jats:italic> reports that ADP released by stressed cells is a signal that triggers HMT.","PeriodicalId":20240,"journal":{"name":"PLoS Biology","volume":null,"pages":null},"PeriodicalIF":9.8,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142225120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-25DOI: 10.1371/journal.pbio.3001767
Melissa D. Parker, Elise S. Brunk, Adam J. Getzler, Katrin Karbstein
The 18S rRNA sequence is highly conserved, particularly at its 3′-end, which is formed by the endonuclease Nob1. How Nob1 identifies its target sequence is not known, and in vitro experiments have shown Nob1 to be error-prone. Moreover, the sequence around the 3′-end is degenerate with similar sites nearby. Here, we used yeast genetics, biochemistry, and next-generation sequencing to investigate a role for the ATPase Rio1 in monitoring the accuracy of the 18S rRNA 3′-end. We demonstrate that Nob1 can miscleave its rRNA substrate and that miscleaved rRNA accumulates upon bypassing the Rio1-mediated quality control (QC) step, but not in healthy cells with intact QC mechanisms. Mechanistically, we show that Rio1 binding to miscleaved rRNA is weaker than its binding to accurately processed 18S rRNA. Accordingly, excess Rio1 results in accumulation of miscleaved rRNA. Ribosomes containing miscleaved rRNA can translate, albeit more slowly, thereby inviting collisions with trailing ribosomes. These collisions result in degradation of the defective ribosomes utilizing parts of the machinery for mRNA QC. Altogether, the data support a model in which Rio1 inspects the 3′-end of the nascent 18S rRNA to prevent miscleaved 18S rRNA-containing ribosomes from erroneously engaging in translation, where they induce ribosome collisions. The data also demonstrate how ribosome collisions purify cells of altered ribosomes with different functionalities, with important implications for the concept of ribosome heterogeneity.
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