Pub Date : 2024-09-03DOI: 10.1101/cshperspect.a041458
Michael Heinzinger, Burkhard Rost
From AlphaGO over StableDiffusion to ChatGPT, the recent decade of exponential advances in artificial intelligence (AI) has been altering life. In parallel, advances in computational biology are beginning to decode the language of life: AlphaFold2 leaped forward in protein structure prediction, and protein language models (pLMs) replaced expertise and evolutionary information from multiple sequence alignments with information learned from reoccurring patterns in databases of billions of proteins without experimental annotations other than the amino acid sequences. None of those tools could have been developed 10 years ago; all will increase the wealth of experimental data and speed up the cycle from idea to proof. AI is affecting molecular and medical biology at giant steps, and the most important might be the leap toward more powerful protein design.
{"title":"Artificial Intelligence Learns Protein Prediction.","authors":"Michael Heinzinger, Burkhard Rost","doi":"10.1101/cshperspect.a041458","DOIUrl":"10.1101/cshperspect.a041458","url":null,"abstract":"<p><p>From <i>AlphaGO</i> over <i>StableDiffusion</i> to <i>ChatGPT</i>, the recent decade of exponential advances in artificial intelligence (AI) has been altering life. In parallel, advances in computational biology are beginning to decode the language of life: <i>AlphaFold2</i> leaped forward in protein structure prediction, and protein language models (pLMs) replaced expertise and evolutionary information from multiple sequence alignments with information learned from reoccurring patterns in databases of billions of proteins without experimental annotations other than the amino acid sequences. None of those tools could have been developed 10 years ago; all will increase the wealth of experimental data and speed up the cycle from idea to proof. AI is affecting molecular and medical biology at giant steps, and the most important might be the leap toward more powerful protein design.</p>","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-03DOI: 10.1101/cshperspect.a041440
Ken A Thompson, Yaniv Brandvain, Jenn M Coughlan, Kira E Delmore, Hannah Justen, Catherine R Linnen, Daniel Ortiz-Barrientos, Catherine A Rushworth, Hilde Schneemann, Molly Schumer, Rike Stelkens
Ecologically mediated selection against hybrids, caused by hybrid phenotypes fitting poorly into available niches, is typically viewed as distinct from selection caused by epistatic Dobzhansky-Muller hybrid incompatibilities. Here, we show how selection against transgressive phenotypes in hybrids manifests as incompatibility. After outlining our logic, we summarize current approaches for studying ecology-based selection on hybrids. We then quantitatively review QTL-mapping studies and find traits differing between parent taxa are typically polygenic. Next, we describe how verbal models of selection on hybrids translate to phenotypic and genetic fitness landscapes, highlighting emerging approaches for detecting polygenic incompatibilities. Finally, in a synthesis of published data, we report that trait transgression-and thus possibly extrinsic hybrid incompatibility in hybrids-escalates with the phenotypic divergence between parents. We discuss conceptual implications and conclude that studying the ecological basis of hybrid incompatibility will facilitate new discoveries about mechanisms of speciation.
{"title":"The Ecology of Hybrid Incompatibilities.","authors":"Ken A Thompson, Yaniv Brandvain, Jenn M Coughlan, Kira E Delmore, Hannah Justen, Catherine R Linnen, Daniel Ortiz-Barrientos, Catherine A Rushworth, Hilde Schneemann, Molly Schumer, Rike Stelkens","doi":"10.1101/cshperspect.a041440","DOIUrl":"10.1101/cshperspect.a041440","url":null,"abstract":"<p><p>Ecologically mediated selection against hybrids, caused by hybrid phenotypes fitting poorly into available niches, is typically viewed as distinct from selection caused by epistatic Dobzhansky-Muller hybrid incompatibilities. Here, we show how selection against transgressive phenotypes in hybrids manifests as incompatibility. After outlining our logic, we summarize current approaches for studying ecology-based selection on hybrids. We then quantitatively review QTL-mapping studies and find traits differing between parent taxa are typically polygenic. Next, we describe how verbal models of selection on hybrids translate to phenotypic and genetic fitness landscapes, highlighting emerging approaches for detecting polygenic incompatibilities. Finally, in a synthesis of published data, we report that trait transgression-and thus possibly extrinsic hybrid incompatibility in hybrids-escalates with the phenotypic divergence between parents. We discuss conceptual implications and conclude that studying the ecological basis of hybrid incompatibility will facilitate new discoveries about mechanisms of speciation.</p>","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139048453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041370
Leon C.D. Smyth, Natalie Beschorner, Maiken Nedergaard, Jonathan Kipnis
Cerebrospinal fluid (CSF) bathes and cushions the brain; however, it also serves a major role in the clearance of metabolic wastes and in the distribution of glucose, lipids, and amino acids. Unlike every other organ in the body, the brain parenchyma lacks a traditional lymphatic system to drain fluids and central nervous system (CNS) antigens. It was historically assumed that all brain wastes were removed by endogenous processing, such as phagocytosis and autophagy, while excess fluids drained directly into the blood. However, the twin discoveries of the glial-lymphatic (glymphatic) system and meningeal lymphatics have transformed our understanding of brain waste clearance. The glymphatic system describes the movement of fluids through the subarachnoid space (SAS), the influx along periarterial spaces into the brain parenchyma, and the ultimate efflux back into the SAS along perivenous spaces where it comes into direct contact with the meningeal lymphatics. The dura mater of the meninges contains a bona fide lymphatic network that can drain CSF that has entered the dura. Together, these pathways provide insights into the clearance of molecules and fluids from the brain, and show that the CNS is physically connected to the adaptive immune system. Here, we outline the glymphatic and lymphatic systems, and describe the cellular components that are important to their function.
{"title":"Cellular Contributions to Glymphatic and Lymphatic Waste Clearance in the Brain","authors":"Leon C.D. Smyth, Natalie Beschorner, Maiken Nedergaard, Jonathan Kipnis","doi":"10.1101/cshperspect.a041370","DOIUrl":"https://doi.org/10.1101/cshperspect.a041370","url":null,"abstract":"Cerebrospinal fluid (CSF) bathes and cushions the brain; however, it also serves a major role in the clearance of metabolic wastes and in the distribution of glucose, lipids, and amino acids. Unlike every other organ in the body, the brain parenchyma lacks a traditional lymphatic system to drain fluids and central nervous system (CNS) antigens. It was historically assumed that all brain wastes were removed by endogenous processing, such as phagocytosis and autophagy, while excess fluids drained directly into the blood. However, the twin discoveries of the glial-lymphatic (glymphatic) system and meningeal lymphatics have transformed our understanding of brain waste clearance. The glymphatic system describes the movement of fluids through the subarachnoid space (SAS), the influx along periarterial spaces into the brain parenchyma, and the ultimate efflux back into the SAS along perivenous spaces where it comes into direct contact with the meningeal lymphatics. The dura mater of the meninges contains a bona fide lymphatic network that can drain CSF that has entered the dura. Together, these pathways provide insights into the clearance of molecules and fluids from the brain, and show that the CNS is physically connected to the adaptive immune system. Here, we outline the glymphatic and lymphatic systems, and describe the cellular components that are important to their function.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041477
Stefano Schiaffino, Francesco Chemello, Carlo Reggiani
The widespread presence of slow-red and fast-white muscles in all vertebrates supports the evolutionary advantage of having two types of motors available for animal movement—a slow economical motor used for most activities, and a fast energetically costly motor used for rapid movements and emergency actions, and actions that require a lot of force. Skeletal muscles are composed of multiple fiber types whose structural and functional properties have only in part been characterized. Further progress in this field is mainly occurring along two directions: Multiomics approaches are providing a global picture of the molecular composition of muscle fibers up to the single fiber and single nucleus level. Signaling studies are identifying many transcription factors and pathways controlling fiber-type specification. These new data should now be integrated into a wider whole-body context by defining the matching between muscle fiber and motor neuron heterogeneity in the neuromuscular system, as well as the relevance of muscle fiber types in systemic homeostatic functions, including metabolism and thermogenesis.
{"title":"The Diversity of Skeletal Muscle Fiber Types","authors":"Stefano Schiaffino, Francesco Chemello, Carlo Reggiani","doi":"10.1101/cshperspect.a041477","DOIUrl":"https://doi.org/10.1101/cshperspect.a041477","url":null,"abstract":"The widespread presence of slow-red and fast-white muscles in all vertebrates supports the evolutionary advantage of having two types of motors available for animal movement—a slow economical motor used for most activities, and a fast energetically costly motor used for rapid movements and emergency actions, and actions that require a lot of force. Skeletal muscles are composed of multiple fiber types whose structural and functional properties have only in part been characterized. Further progress in this field is mainly occurring along two directions: Multiomics approaches are providing a global picture of the molecular composition of muscle fibers up to the single fiber and single nucleus level. Signaling studies are identifying many transcription factors and pathways controlling fiber-type specification. These new data should now be integrated into a wider whole-body context by defining the matching between muscle fiber and motor neuron heterogeneity in the neuromuscular system, as well as the relevance of muscle fiber types in systemic homeostatic functions, including metabolism and thermogenesis.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041457
Anjana Sevagamoorthy, Adeline Vanderver, Jamie L. Fraser, Jennifer Orthmann-Murphy
Inherited white matter disorders (IWMDs) are a phenotypically and genotypically heterogeneous group of disorders affecting the central nervous system (CNS) with or without peripheral neuropathy. They are classified either as leukodystrophies (LDs), with primary glial abnormalities, or genetic leukoencephalopathies (gLEs), where other CNS cells are involved. As a group, these disorders are common, with an incidence of 1 in 7500 births. However, IWMDs often go undiagnosed or suffer delayed or misdiagnosis due to their heterogeneous presentation. Many of these disorders present with lethal secondary manifestations that can be prevented through early disease recognition, periodic surveillance, and preventative management. Emerging therapeutics, including gene therapy trials for metachromatic leukodystrophy (MLD) and adrenoleukodystrophy (ALD), suggest disease progression may be slowed or even prevented if treated early. Therapies for IWMDs that target glial cells or the peripheral immune system may provide novel insights for treating acquired disorders of white matter.
{"title":"Glial Origins of Inherited White Matter Disorders","authors":"Anjana Sevagamoorthy, Adeline Vanderver, Jamie L. Fraser, Jennifer Orthmann-Murphy","doi":"10.1101/cshperspect.a041457","DOIUrl":"https://doi.org/10.1101/cshperspect.a041457","url":null,"abstract":"Inherited white matter disorders (IWMDs) are a phenotypically and genotypically heterogeneous group of disorders affecting the central nervous system (CNS) with or without peripheral neuropathy. They are classified either as leukodystrophies (LDs), with primary glial abnormalities, or genetic leukoencephalopathies (gLEs), where other CNS cells are involved. As a group, these disorders are common, with an incidence of 1 in 7500 births. However, IWMDs often go undiagnosed or suffer delayed or misdiagnosis due to their heterogeneous presentation. Many of these disorders present with lethal secondary manifestations that can be prevented through early disease recognition, periodic surveillance, and preventative management. Emerging therapeutics, including gene therapy trials for metachromatic leukodystrophy (MLD) and adrenoleukodystrophy (ALD), suggest disease progression may be slowed or even prevented if treated early. Therapies for IWMDs that target glial cells or the peripheral immune system may provide novel insights for treating acquired disorders of white matter.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041565
Anais Franco-Romero, Marco Sandri, Stefano Schiaffino
Skeletal muscle fibers possess, like all cells of our body, an evolutionary conserved autophagy machinery, which allows them to segregate unfolded proteins and damaged organelles within autophagosomes, and to induce fusion of autophagosomes with lysosomes, leading to degradation of those altered cell constituents. This process may be selective for specific cell components, as in the case of glycogen (glycophagy) or organelles, as with mitochondria (mitophagy). The autophagic flux is activated by fasting, and contributes with the proteasome to provide the organism with amino acids required for survival. Autophagy is also essential for the normal turnover of muscle proteins and organelles, as shown by the degenerative changes induced by genetic block of the autophagic mechanism, and in several myopathies. Autophagy is enhanced in muscle by exercise and impaired during aging, suggesting that aging-dependent muscle dysfunction could be delayed by boosting autophagy.
{"title":"Autophagy in Skeletal Muscle","authors":"Anais Franco-Romero, Marco Sandri, Stefano Schiaffino","doi":"10.1101/cshperspect.a041565","DOIUrl":"https://doi.org/10.1101/cshperspect.a041565","url":null,"abstract":"Skeletal muscle fibers possess, like all cells of our body, an evolutionary conserved autophagy machinery, which allows them to segregate unfolded proteins and damaged organelles within autophagosomes, and to induce fusion of autophagosomes with lysosomes, leading to degradation of those altered cell constituents. This process may be selective for specific cell components, as in the case of glycogen (glycophagy) or organelles, as with mitochondria (mitophagy). The autophagic flux is activated by fasting, and contributes with the proteasome to provide the organism with amino acids required for survival. Autophagy is also essential for the normal turnover of muscle proteins and organelles, as shown by the degenerative changes induced by genetic block of the autophagic mechanism, and in several myopathies. Autophagy is enhanced in muscle by exercise and impaired during aging, suggesting that aging-dependent muscle dysfunction could be delayed by boosting autophagy.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041500
Abigail L. Mackey
A critical link in the chain of force transmission from muscle fiber cross-bridge to bone is the interface between muscle and tendon—the myotendinous junction (MTJ). To meet the challenge of connecting these two tissues, the MTJ is specialized molecularly and morphologically. Distinct transcriptional profiles are evident for the myonuclei at the myofiber tips and a population of mononuclear tendon cells at the MTJ, demonstrating support from both sides in MTJ maintenance. Paradoxically, despite this high degree of specialization, the MTJ remains susceptible to strain (rupture) injury and is often associated with failed tissue healing. Incomplete understanding of the nature of the MTJ and the elements contributing to its plasticity hinder tackling this unsolved clinical challenge. The goal of this review is to summarize key structural and molecular features of the MTJ, discuss MTJ adaptation in response to mechanical (un)loading, aging, and injury, and highlight the major unanswered questions surrounding the MTJ.
{"title":"The Myotendinous Junction—Form and Function","authors":"Abigail L. Mackey","doi":"10.1101/cshperspect.a041500","DOIUrl":"https://doi.org/10.1101/cshperspect.a041500","url":null,"abstract":"A critical link in the chain of force transmission from muscle fiber cross-bridge to bone is the interface between muscle and tendon—the myotendinous junction (MTJ). To meet the challenge of connecting these two tissues, the MTJ is specialized molecularly and morphologically. Distinct transcriptional profiles are evident for the myonuclei at the myofiber tips and a population of mononuclear tendon cells at the MTJ, demonstrating support from both sides in MTJ maintenance. Paradoxically, despite this high degree of specialization, the MTJ remains susceptible to strain (rupture) injury and is often associated with failed tissue healing. Incomplete understanding of the nature of the MTJ and the elements contributing to its plasticity hinder tackling this unsolved clinical challenge. The goal of this review is to summarize key structural and molecular features of the MTJ, discuss MTJ adaptation in response to mechanical (un)loading, aging, and injury, and highlight the major unanswered questions surrounding the MTJ.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-12DOI: 10.1101/cshperspect.a041361
Matthew N. Rasband, Elior Peles
Action potential propagation along myelinated axons requires clustered voltage-gated sodium and potassium channels. These channels must be restricted to nodes of Ranvier where the action potential is regenerated. Several mechanisms have evolved to facilitate and ensure the correct assembly and stabilization of these essential axonal domains. This review highlights the current understanding of the axon-intrinsic and glial-extrinsic mechanisms that control the formation and maintenance of the nodes of Ranvier in both the peripheral (PNS) and central (CNS) nervous systems.
{"title":"The Nodes of Ranvier: Mechanisms of Assembly and Maintenance","authors":"Matthew N. Rasband, Elior Peles","doi":"10.1101/cshperspect.a041361","DOIUrl":"https://doi.org/10.1101/cshperspect.a041361","url":null,"abstract":"Action potential propagation along myelinated axons requires clustered voltage-gated sodium and potassium channels. These channels must be restricted to nodes of Ranvier where the action potential is regenerated. Several mechanisms have evolved to facilitate and ensure the correct assembly and stabilization of these essential axonal domains. This review highlights the current understanding of the axon-intrinsic and glial-extrinsic mechanisms that control the formation and maintenance of the nodes of Ranvier in both the peripheral (PNS) and central (CNS) nervous systems.","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":7.2,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141933439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1101/cshperspect.a041352
Won-Suk Chung, Katherine T Baldwin, Nicola J Allen
Astrocytes play an integral role in the development, maturation, and refinement of neuronal circuits. Astrocytes secrete proteins and lipids that instruct the formation of new synapses and induce the maturation of existing synapses. Through contact-mediated signaling, astrocytes can regulate the formation and state of synapses within their domain. Through phagocytosis, astrocytes participate in the elimination of excess synaptic connections. In this work, we will review key findings on the molecular mechanisms of astrocyte-synapse interaction with a focus on astrocyte-secreted factors, contact-mediated mechanisms, and synapse elimination. We will discuss this in the context of typical brain development and maintenance, as well as consider the consequences of dysfunction in these pathways in neurological disorders, highlighting a role for astrocytes in health and disease.
{"title":"Astrocyte Regulation of Synapse Formation, Maturation, and Elimination.","authors":"Won-Suk Chung, Katherine T Baldwin, Nicola J Allen","doi":"10.1101/cshperspect.a041352","DOIUrl":"10.1101/cshperspect.a041352","url":null,"abstract":"<p><p>Astrocytes play an integral role in the development, maturation, and refinement of neuronal circuits. Astrocytes secrete proteins and lipids that instruct the formation of new synapses and induce the maturation of existing synapses. Through contact-mediated signaling, astrocytes can regulate the formation and state of synapses within their domain. Through phagocytosis, astrocytes participate in the elimination of excess synaptic connections. In this work, we will review key findings on the molecular mechanisms of astrocyte-synapse interaction with a focus on astrocyte-secreted factors, contact-mediated mechanisms, and synapse elimination. We will discuss this in the context of typical brain development and maintenance, as well as consider the consequences of dysfunction in these pathways in neurological disorders, highlighting a role for astrocytes in health and disease.</p>","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1101/cshperspect.a041713
Robert G Parton, Kai Simons
Lipids are the defining features of cellular membranes. They act collectively to form a variety of different structures, and understanding their complex behavior represents an early example of systems biology. A multidisciplinary approach is needed to analyse the functions of lipids in biological systems, and new work is providing fascinating insights into their roles in membrane biology, metabolism, signaling, subcellular dynamics and various disease processes.
{"title":"The Biology of Lipids.","authors":"Robert G Parton, Kai Simons","doi":"10.1101/cshperspect.a041713","DOIUrl":"10.1101/cshperspect.a041713","url":null,"abstract":"<p><p>Lipids are the defining features of cellular membranes. They act collectively to form a variety of different structures, and understanding their complex behavior represents an early example of systems biology. A multidisciplinary approach is needed to analyse the functions of lipids in biological systems, and new work is providing fascinating insights into their roles in membrane biology, metabolism, signaling, subcellular dynamics and various disease processes.</p>","PeriodicalId":10494,"journal":{"name":"Cold Spring Harbor perspectives in biology","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139691426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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