scholarly journals Plant evolution driven by interactions with symbiotic and pathogenic microbes

Science ◽  
2021 ◽  
Vol 371 (6531) ◽  
pp. eaba6605 ◽  
Author(s):  
Pierre-Marc Delaux ◽  
Sebastian Schornack
Keyword(s):  
Cell Biology ◽  
Genetic Basis ◽  
Reverse Genetics ◽  
Molecular Mechanisms ◽  
Plant Evolution ◽  
Symbiotic Microorganisms ◽  
Protection Mechanisms ◽  
Evolutionary Trajectories ◽  
Microbe Interactions ◽  
Pathogenic Microbes

During 450 million years of diversification on land, plants and microbes have evolved together. This is reflected in today’s continuum of associations, ranging from parasitism to mutualism. Through phylogenetics, cell biology, and reverse genetics extending beyond flowering plants into bryophytes, scientists have started to unravel the genetic basis and evolutionary trajectories of plant-microbe associations. Protection against pathogens and support of beneficial, symbiotic, microorganisms are sustained by a blend of conserved and clade-specific plant mechanisms evolving at different speeds. We propose that symbiosis consistently emerges from the co-option of protection mechanisms and general cell biology principles. Exploring and harnessing the diversity of molecular mechanisms used in nonflowering plant-microbe interactions may extend the possibilities for engineering symbiosis-competent and pathogen-resilient crops.

scholarly journals Alternate histories of cytokinesis: lessons from the trypanosomatids

2020 ◽  
Vol 31 (24) ◽  
pp. 2631-2639
Author(s):  
Paul C. Campbell ◽  
Christopher L. de Graffenried
Keyword(s):  
Cell Biology ◽  
Molecular Mechanisms ◽  
Sparse Sampling ◽  
Model Organisms ◽  
Great Success ◽  
Eukaryotic Diversity ◽  
Daughter Cells ◽  
Evolutionary Trajectories ◽  
Unicellular Organisms ◽  
Cellular Organelles

Popular culture has recently produced several “alternate histories” that describe worlds where key historical events had different outcomes. Beyond entertainment, asking “could this have happened a different way?” and “what would the consequences be?” are valuable approaches for exploring molecular mechanisms in many areas of research, including cell biology. Analogous to alternate histories, studying how the evolutionary trajectories of related organisms have been selected to provide a range of outcomes can tell us about the plasticity and potential contained within the genome of the ancestral cell. Among eukaryotes, a group of model organisms has been employed with great success to identify a core, conserved framework of proteins that segregate the duplicated cellular organelles into two daughter cells during cell division, a process known as cytokinesis. However, these organisms provide relatively sparse sampling across the broad evolutionary distances that exist, which has limited our understanding of the true potential of the ancestral eukaryotic toolkit. Recent work on the trypanosomatids, a group of eukaryotic parasites, exemplifies alternate historical routes for cytokinesis that illustrate the range of eukaryotic diversity, especially among unicellular organisms.

Home sweet home – how mutualistic microbes modify root development to promote symbiosis

2020 ◽  
Author(s):  
Mina Ghahremani ◽  
Allyson M MacLean
Keyword(s):  
Root Development ◽  
Cell Biology ◽  
Developmental Plasticity ◽  
Molecular Mechanisms ◽  
General Knowledge ◽  
Cortical Cells ◽  
Specific Manner ◽  
Organism Growth ◽  
Microbe Interactions ◽  
Developmentally Responsive

Abstract Post-embryonic organogenesis has uniquely equipped plants to become developmentally responsive to their environment, affording opportunities to remodel organism growth and architecture to an extent not possible in other higher order eukaryotes. It is this developmental plasticity that makes the field of plant-microbe interactions an exceptionally fascinating venue in which to study symbiosis. This review article describes the various ways in which mutualistic microbes alter the growth, development, and architecture of the roots of their plant hosts. We first summarize general knowledge of root development, and then examine how association of plants with beneficial microbes affects these processes. Working our way inwards from the epidermis to the pericycle, this review dissects the cell biology and molecular mechanisms underlying plant-microbe interactions in a tissue-specific manner. We examine the ways in which microbes gain entry into the root, and modify this specialized organ for symbiont accommodation, with a particular emphasis on the colonization of root cortical cells. We present significant advances in our understanding of root-microbe interactions, and conclude our discussion by identifying questions pertinent to root endosymbiosis that at present remain unresolved.

scholarly journals Isolation of Natural Fungal Pathogens from Marchantia polymorpha Reveals Antagonism between Salicylic Acid and Jasmonate during Liverwort–Fungus Interactions

2019 ◽  
Vol 61 (2) ◽  
pp. 265-275 ◽  
Author(s):  
Hidenori Matsui ◽  
Hidekazu Iwakawa ◽  
Gang-Su Hyon ◽  
Izumi Yotsui ◽  
Shinpei Katou ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Fungal Pathogens ◽  
Molecular Mechanisms ◽  
Land Plant ◽  
Plant Evolution ◽  
Marchantia Polymorpha ◽  
Bjerkandera Adusta ◽  
Irpex Lacteus ◽  
Microbe Interactions ◽  
Land Plant Evolution

Abstract The evolution of adaptive interactions with beneficial, neutral and detrimental microbes was one of the key features enabling plant terrestrialization. Extensive studies have revealed conserved and unique molecular mechanisms underlying plant–microbe interactions across different plant species; however, most insights gleaned to date have been limited to seed plants. The liverwort Marchantia polymorpha, a descendant of early diverging land plants, is gaining in popularity as an advantageous model system to understand land plant evolution. However, studying evolutionary molecular plant–microbe interactions in this model is hampered by the small number of pathogens known to infect M. polymorpha. Here, we describe four pathogenic fungal strains, Irpex lacteus Marchantia-infectious (MI)1, Phaeophlebiopsis peniophoroides MI2, Bjerkandera adusta MI3 and B. adusta MI4, isolated from diseased M. polymorpha. We demonstrate that salicylic acid (SA) treatment of M. polymorpha promotes infection of the I. lacteus MI1 that is likely to adopt a necrotrophic lifestyle, while this effect is suppressed by co-treatment with the bioactive jasmonate in M. polymorpha, dinor-cis-12-oxo-phytodienoic acid (dn-OPDA), suggesting that antagonistic interactions between SA and oxylipin pathways during plant–fungus interactions are ancient and were established already in liverworts.

Molecular Basis and Clinical Aspects of Hereditary Megakaryocyte and Platelet Membrane Glycoprotein Disorders

1996 ◽  
Vol 16 (02) ◽  
pp. 114-138 ◽  
Author(s):  
R. E. Scharf
Keyword(s):  
Genetic Basis ◽  
Molecular Mechanisms ◽  
Molecular Genetic ◽  
Platelet Membrane ◽  
Clinical Aspects ◽  
Membrane Glycoprotein ◽  
Membrane Glycoproteins ◽  
Membrane Expression ◽  
Receptor Complexes ◽  
Platelet Membrane Glycoprotein

SummarySpecific membrane glycoproteins (GP) expressed by the megakaryocyte-platelet system, including GPIa-lla, GPIb-V-IX, GPIIb-llla, and GPIV are involved in mediat-ing platelet adhesion to the subendothelial matrix. Among these glycoproteins, GPIIb-llla plays a pivotal role since platelet aggregation is exclusively mediated by this receptor and its interaction with soluble macromolecular proteins. Inherited defects of the GPIIb-llla or GPIb-V-IX receptor complexes are associated with bleeding disorders, known as Glanzmann's thrombasthenia, Bernard-Soulier syndrome, or platelet-type von Willebrand's disease, respectively. Using immuno-chemical and molecular biology techniques, rapid advances in our understanding of the molecular genetic basis of these disorders have been made during the last few years. Moreover, analyses of patients with congenital platelet membrane glycoprotein abnormalities have provided valuable insights into molecular mechanisms that are required for structural and functional integrity, normal biosynthesis of the glycoprotein complexes and coordinated membrane expression of their constituents. The present article reviews the current state of knowledge of the major membrane glycoproteins in health and disease. The spectrum of clinical bleeding manifestations and established diagnostic criteria for each of these dis-orders are summarized. In particular, the variety of molecular defects that have been identified so far and their genetic basis will be discussed.

scholarly journals Molecular regulation of Snai2 in development and disease

2019 ◽  
Vol 132 (23) ◽  
Author(s):  
Wenhui Zhou ◽  
Kayla M. Gross ◽  
Charlotte Kuperwasser
Keyword(s):  
Transcription Factor ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Zinc Finger Protein ◽  
Main Role ◽  
Biological Processes ◽  
Developmental Defects ◽  
Mesenchymal Transition ◽  
Damage Repair

ABSTRACT The transcription factor Snai2, encoded by the SNAI2 gene, is an evolutionarily conserved C2H2 zinc finger protein that orchestrates biological processes critical to tissue development and tumorigenesis. Initially characterized as a prototypical epithelial-to-mesenchymal transition (EMT) transcription factor, Snai2 has been shown more recently to participate in a wider variety of biological processes, including tumor metastasis, stem and/or progenitor cell biology, cellular differentiation, vascular remodeling and DNA damage repair. The main role of Snai2 in controlling such processes involves facilitating the epigenetic regulation of transcriptional programs, and, as such, its dysregulation manifests in developmental defects, disruption of tissue homeostasis, and other disease conditions. Here, we discuss our current understanding of the molecular mechanisms regulating Snai2 expression, abundance and activity. In addition, we outline how these mechanisms contribute to disease phenotypes or how they may impact rational therapeutic targeting of Snai2 dysregulation in human disease.

scholarly journals Physical Exercise and Cardiac Repair: The Potential Role of Nitric Oxide in Boosting Stem Cell Regenerative Biology

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1002
Author(s):  
Fabiola Marino ◽  
Mariangela Scalise ◽  
Eleonora Cianflone ◽  
Luca Salerno ◽  
Donato Cappetta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stem Cell ◽  
Physical Exercise ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Heart Function ◽  
Stem Cell Biology ◽  
Myocardial Repair ◽  
Beneficial Effects

Over the years strong evidence has been accumulated showing that aerobic physical exercise exerts beneficial effects on the prevention and reduction of cardiovascular risk. Exercise in healthy subjects fosters physiological remodeling of the adult heart. Concurrently, physical training can significantly slow-down or even reverse the maladaptive pathologic cardiac remodeling in cardiac diseases, improving heart function. The underlying cellular and molecular mechanisms of the beneficial effects of physical exercise on the heart are still a subject of intensive study. Aerobic activity increases cardiovascular nitric oxide (NO) released mainly through nitric oxidase synthase 3 activity, promoting endothelium-dependent vasodilation, reducing vascular resistance, and lowering blood pressure. On the reverse, an imbalance between increasing free radical production and decreased NO generation characterizes pathologic remodeling, which has been termed the “nitroso-redox imbalance”. Besides these classical evidence on the role of NO in cardiac physiology and pathology, accumulating data show that NO regulate different aspects of stem cell biology, including survival, proliferation, migration, differentiation, and secretion of pro-regenerative factors. Concurrently, it has been shown that physical exercise generates physiological remodeling while antagonizes pathologic remodeling also by fostering cardiac regeneration, including new cardiomyocyte formation. This review is therefore focused on the possible link between physical exercise, NO, and stem cell biology in the cardiac regenerative/reparative response to physiological or pathological load. Cellular and molecular mechanisms that generate an exercise-induced cardioprotective phenotype are discussed in regards with myocardial repair and regeneration. Aerobic training can benefit cells implicated in cardiovascular homeostasis and response to damage by NO-mediated pathways that protect stem cells in the hostile environment, enhance their activation and differentiation and, in turn, translate to more efficient myocardial tissue regeneration. Moreover, stem cell preconditioning by and/or local potentiation of NO signaling can be envisioned as promising approaches to improve the post-transplantation stem cell survival and the efficacy of cardiac stem cell therapy.

scholarly journals Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Tsui-Wen Chou ◽  
Nydia P. Chang ◽  
Medha Krishnagiri ◽  
Aisha P. Patel ◽  
Marissa Lindman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Neuronal Cell ◽  
Dopamine Neurons ◽  
Functional Markers ◽  
Kinase Signaling ◽  
Astrocyte Activation ◽  
Transcriptional Responses

AbstractParkinson’s disease (PD) is a neurodegenerative disorder characterized by the death of midbrain dopamine neurons. The pathogenesis of PD is poorly understood, though misfolded and/or aggregated forms of the protein α-synuclein have been implicated in several neurodegenerative disease processes, including neuroinflammation and astrocyte activation. Astrocytes in the midbrain play complex roles during PD, initiating both harmful and protective processes that vary over the course of the disease. However, despite their significant regulatory roles during neurodegeneration, the cellular and molecular mechanisms that promote pathogenic astrocyte activity remain mysterious. Here, we show that α-synuclein preformed fibrils (PFFs) induce pathogenic activation of human midbrain astrocytes, marked by inflammatory transcriptional responses, downregulation of phagocytic function, and conferral of neurotoxic activity. These effects required the necroptotic kinases RIPK1 and RIPK3, but were independent of MLKL and necroptosis. Instead, both transcriptional and functional markers of astrocyte activation occurred via RIPK-dependent activation of NF-κB signaling. Our study identifies a previously unknown function for α-synuclein in promoting neurotoxic astrocyte activation, as well as new cell death-independent roles for RIP kinase signaling in the regulation of glial cell biology and neuroinflammation. Together, these findings highlight previously unappreciated molecular mechanisms of pathologic astrocyte activation and neuronal cell death with implications for Parkinsonian neurodegeneration.

scholarly journals Interrogating Plant-Microbe Interactions with Chemical Tools: Click Chemistry Reagents for Metabolic Labeling and Activity-Based Probes

Molecules ◽  
2021 ◽  
Vol 26 (1) ◽  
pp. 243
Author(s):  
Vivian S. Lin
Keyword(s):  
Plant Growth ◽  
Immune Responses ◽  
Click Chemistry ◽  
Chemical Biology ◽  
Molecular Mechanisms ◽  
Metabolic Labeling ◽  
Beneficial Microbes ◽  
Plant Hosts ◽  
Microbe Interactions ◽  
Growth Metabolism

Continued expansion of the chemical biology toolbox presents many new and diverse opportunities to interrogate the fundamental molecular mechanisms driving complex plant–microbe interactions. This review will examine metabolic labeling with click chemistry reagents and activity-based probes for investigating the impacts of plant-associated microbes on plant growth, metabolism, and immune responses. While the majority of the studies reviewed here used chemical biology approaches to examine the effects of pathogens on plants, chemical biology will also be invaluable in future efforts to investigate mutualistic associations between beneficial microbes and their plant hosts.

scholarly journals Can artificially selected phenotypes influence a component of field fitness? Thermal selection and fly performance under thermal extremes

2006 ◽  
Vol 274 (1611) ◽  
pp. 771-778 ◽  
Author(s):  
Torsten Nygaard Kristensen ◽  
Volker Loeschcke ◽  
Ary A Hoffmann
Keyword(s):  
High Performance ◽  
Quantitative Traits ◽  
Genetic Basis ◽  
Selected Lines ◽  
Resistant Lines ◽  
Correlated Patterns ◽  
Different Temperatures ◽  
Evolutionary Trajectories ◽  
Low Performance ◽  
Selected Traits

Artificially selected lines are widely used to investigate the genetic basis of quantitative traits and make inferences about evolutionary trajectories. Yet, the relevance of selected traits to field fitness is rarely tested. Here, we assess the relevance of thermal stress resistance artificially selected in the laboratory to one component of field fitness by investigating the likelihood of adult Drosophila melanogaster reaching food bait under different temperatures. Lines resistant to heat reached the bait more often than controls under hot and cold conditions, but less often at intermediate temperatures, suggesting a fitness cost of increased heat resistance but not at temperature extremes. Cold-resistant lines were more common at baits than controls under cold as well as hot field conditions, and there was no cost at intermediate temperatures. One of the replicate heat-resistant lines was caught less often than the others under hot conditions. Direct and correlated patterns of responses in laboratory tests did not fully predict the low performance of the heat selected lines at intermediate temperatures, nor the high performance of the cold selected lines under hot conditions. Therefore, lines selected artificially not only behaved partly as expected based on laboratory assays but also evolved patterns only evident in the field releases.

Cell Biology and Molecular Mechanisms in Artificial Device Infections

1993 ◽  
Vol 16 (11) ◽  
pp. 755-764 ◽  
Author(s):  
A.G. Gristina ◽  
G. Giridhar ◽  
B.L Gabriel ◽  
P.T. Naylor ◽  
Q.N. Myrvik
Keyword(s):  
Bacterial Adhesion ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Total Joint Replacement ◽  
Total Artificial Heart ◽  
Implant Surface ◽  
Microbial Adhesion ◽  
Major Barrier ◽  
Tissue Integration ◽  
Biomaterial Surfaces

Biomaterials are being used with increasing frequency for tissue substitution. Complex devices such as total joint replacement and the total artificial heart represent combinations of polymers and metal alloys for system and organ replacement. The major barrier to the extended use of these devices is bacterial adhesion to biomaterials, which causes biomaterial-centered infection, and the lack of successful tissue integration or compatibility with biomaterial surfaces. Adhesion-mediated infections are extremely resistant to antibiotics and host defenses and frequently persist until the biomaterial or foreign body is removed. The pathogenesis of adhesive infections is related, in part, to preferential colonization of “inert” substrata whose surfaces are not integrated with healthy tissues composed of living cells and intact extracellular polymers. Tissue integration is an interesting parallel to microbial adhesion and is a desired phenomenon for the biocompatibility of certain implants and biomaterials. Tissue integration requires a form of eukaryocytic adhesion or compatibility with possible chemical integration to an implant surface. Many of the fundamental principles of interfacial science apply to both microbial adhesion and to tissue integration and are general to and independent of the substratum materials involved. Interactions of biomaterials with bacteria and tissue cells are directed not only by specific receptors and outer membrane molecules on the cell surface, but also by the atomic geometry and electronic state of the biomaterial surface. An understanding of these mechanisms is important to all fields of medicine and is derived from and relevant to studies in microbiology, biochemistry, and physics. Modifications of biomaterial surfaces at an atomic level will allow the programming of cell-to-substratum events, thereby diminishing infection by enhancing tissue compatibility or integration, or by directly inhibiting bacterial adhesion.

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