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 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 The Ca2+ sensor protein CMI1 fine tunes root development, auxin distribution and responses

2018 ◽  
Author(s):  
Ora Hazak ◽  
Elad Mamon ◽  
Meirav Lavy ◽  
Hasana Sternberg ◽  
Smrutisanjita Behera ◽  
...  
Keyword(s):  
Root Growth ◽  
Root Development ◽  
Lateral Root ◽  
Developmental Plasticity ◽  
Molecular Mechanisms ◽  
Ectopic Expression ◽  
Growth Arrest ◽  
Root Hairs ◽  
Root Tip ◽  
Auxin Distribution

Signaling cross-talks between auxin, a regulator of plant development and Ca2+, a universal second messenger have been proposed to modulate developmental plasticity in plants. However, the underlying molecular mechanisms are largely unknown. Here we report that in Arabidopsis roots, auxin elicits specific Ca2+ signaling pattern that spatially coincide with the expression pattern of auxin-regulated genes. We identified the EF-hand protein CMI1 (Ca2+ sensor Modulator of ICR1) as an interactor of the ROP effector ICR1 (Interactor of Constitutively active ROP). CMI1 is monomeric in solution, changes its secondary structure at Ca2+ concentrations ranging from 10-9 to 10-8 M and its interaction with ICR1 is Ca2+ dependent, involving a conserved hydrophobic pocket. cmi1 mutants display an increased auxin response including shorter primary roots, longer root hairs, longer hypocotyls and altered lateral root formation while ectopic expression of CMI1 induces root growth arrest and reduced auxin responses at the root tip. When expressed alone, CMI1 is localized at the plasma membrane, the cytoplasm and in nuclei. Interaction of CMI1 and ICR1 results in exclusion of CMI1 from nuclei and suppression of the root growth arrest. CMI1 expression is directly upregulated by auxin while expression of auxin induced genes is enhanced in cmi1 concomitantly with repression of auxin induced Ca2+ increases in the lateral root cap and vasculature, indicating that CMI1 represses early auxin responses. Collectively, our findings identify a crucial function of Ca2+ signaling and CMI1 in root growth and suggest an auxin-Ca2+ regulatory feedback loop that fine tunes root development.

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 Steroidal Regulation of Oviductal microRNAs Is Associated with microRNA-Processing in Beef Cows

2021 ◽  
Vol 22 (2) ◽  
pp. 953
Author(s):  
Angela Maria Gonella-Diaza ◽  
Everton Lopes ◽  
Kauê Ribeiro da Silva ◽  
Ricardo Perecin Nociti ◽  
Gabriella Mamede Andrade ◽  
...  
Keyword(s):  
Mirna Expression ◽  
Sex Steroids ◽  
Molecular Mechanisms ◽  
Beef Cows ◽  
Early Embryo ◽  
Preovulatory Follicle ◽  
Large Follicle ◽  
Specific Manner ◽  
Microrna Processing ◽  
Small Follicle

Information on molecular mechanisms through which sex-steroids regulate oviductal function to support early embryo development is lacking. Here, we hypothesized that the periovulatory endocrine milieu affects the miRNA processing machinery and miRNA expression in bovine oviductal tissues. Growth of the preovulatory follicle was controlled to obtain cows that ovulated a small follicle (SF) and subsequently bore a small corpus luteum (CL; SF-SCL) or a large follicle (LF) and large CL (LF-LCL). These groups differed in the periovulatory plasmatic sex-steroid’s concentrations. Ampulla and isthmus samples were collected on day four of the estrous cycle. Abundance of DROSHA, DICER1, and AGO4 transcripts was greater in the ampulla than the isthmus. In the ampulla, transcription of these genes was greater for the SF-SCL group, while the opposite was observed in the isthmus. The expression of the 88 most abundant miRNAs and 14 miRNAs in the ampulla and 34 miRNAs in isthmus were differentially expressed between LF-LCL and SF-SCL groups. Integration of transcriptomic and miRNA data and molecular pathways enrichment showed that important pathways were inhibited in the SF-SCL group due to miRNA control. In conclusion, the endocrine milieu affects the miRNA expression in the bovine oviduct in a region-specific manner.

scholarly journals Maternal Ethanol Exposure Acutely Elevates Src Family Kinase Activity in the Fetal Cortex

2021 ◽  
Author(s):  
Dandan Wang ◽  
Brian W. Howell ◽  
Eric C. Olson
Keyword(s):  
Tyrosine Phosphorylation ◽  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Src Family Kinase ◽  
Cortical Cells ◽  
Signaling Systems ◽  
Sustained Reduction ◽  
Reelin Signaling

AbstractFetal alcohol syndrome (FAS) is characterized by disrupted fetal brain development and postnatal cognitive impairment. The targets of alcohol are diverse, and it is not clear whether there are common underlying molecular mechanisms producing these disruptions. Prior work established that acute ethanol exposure causes a transient increase in tyrosine phosphorylation of multiple proteins in cultured embryonic cortical cells. In this study, we show that a similar tyrosine phosphorylation transient occurs in the fetal brain after maternal dosing with ethanol. Using phospho-specific antibodies and immunohistochemistry, we mapped regions of highest tyrosine phosphorylation in the fetal cerebral cortex and found that areas of dendritic and axonal growth showed elevated tyrosine phosphorylation 10 min after maternal ethanol exposure. These were also areas of Src expression and Src family kinase (SFK) activation loop phosphorylation (pY416) expression. Importantly, maternal pretreatment with the SFK inhibitor dasatinib completely prevents both the pY416 increase and the tyrosine phosphorylation response. The phosphorylation response was observed in the perisomatic region and neurites of immature migrating and differentiating primary neurons. Importantly, the initial phosphotyrosine transient (~ 30 min) targets both Src and Dab1, two critical elements in Reelin signaling, a pathway required for normal cortical development. This initial phosphorylation response is followed by sustained reduction in Ser3 phosphorylation of n-cofilin, a critical actin severing protein and an identified downstream effector of Reelin signaling. This biochemical disruption is associated with sustained reduction of F-actin content and disrupted Golgi apparatus morphology in developing cortical neurons. The finding outlines a model in which the initial activation of SFKs by ethanol has the potential to disrupt multiple developmentally important signaling systems for several hours after maternal exposure.

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.

Lateral root formation and nutrients: nitrogen in the spotlight

2021 ◽  
Author(s):  
Pierre-Mathieu Pélissier ◽  
Hans Motte ◽  
Tom Beeckman
Keyword(s):  
Signaling Pathways ◽  
Root System ◽  
Root Development ◽  
Lateral Root ◽  
Molecular Mechanisms ◽  
Root Formation ◽  
Lateral Roots ◽  
Nutrient Use Efficiency ◽  
Lateral Root Formation ◽  
Lateral Root Development

Abstract Lateral roots are important to forage for nutrients due to their ability to increase the uptake area of a root system. Hence, it comes as no surprise that lateral root formation is affected by nutrients or nutrient starvation, and as such contributes to the root system plasticity. Understanding the molecular mechanisms regulating root adaptation dynamics towards nutrient availability is useful to optimize plant nutrient use efficiency. There is at present a profound, though still evolving, knowledge on lateral root pathways. Here, we aimed to review the intersection with nutrient signaling pathways to give an update on the regulation of lateral root development by nutrients, with a particular focus on nitrogen. Remarkably, it is for most nutrients not clear how lateral root formation is controlled. Only for nitrogen, one of the most dominant nutrients in the control of lateral root formation, the crosstalk with multiple key signals determining lateral root development is clearly shown. In this update, we first present a general overview of the current knowledge of how nutrients affect lateral root formation, followed by a deeper discussion on how nitrogen signaling pathways act on different lateral root-mediating mechanisms for which multiple recent studies yield insights.

Age- and stage-specific regulation patterns in the hematopoietic stem cell hierarchy

Blood ◽  
2001 ◽  
Vol 98 (10) ◽  
pp. 2966-2972 ◽  
Author(s):  
Hartmut Geiger ◽  
Jarrod M. True ◽  
Gerald de Haan ◽  
Gary Van Zant
Keyword(s):  
Linkage Analysis ◽  
Molecular Mechanisms ◽  
Hematopoietic Stem ◽  
Cell Compartments ◽  
Quantitative Trait Linkage Analysis ◽  
Specific Manner ◽  
Stem And Progenitor Cells ◽  
Specific Regulation ◽  
Stem Cell Hierarchy

Abstract The molecular mechanisms that regulate self-renewal and differentiation of very primitive hematopoietic stem and progenitor cells in vivo are still poorly understood. Despite the clinical relevance, even less is known about the mechanisms that regulate these cells in old animals. In a forward genetic approach, using quantitative trait linkage analysis in the mouse BXD recombinant inbred set, this study identified loci that regulate the genetic variation in the size of primitive hematopoietic cell compartments of young and old C57BL6 and DBA/2 animals. Linked loci were confirmed through the generation and analysis of congenic animals. In addition, a comparative linkage analysis revealed that the number of primitive hematopoietic cells and hematopoietic stem cells are regulated in a stage-specific and an age-specific manner.

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