scholarly journals From element to development: the power of the essential micronutrient boron to shape morphological processes in plants

2020 ◽  
Vol 71 (5) ◽  
pp. 1681-1693 ◽  
Author(s):  
Michaela S Matthes ◽  
Janlo M Robil ◽  
Paula McSteen
Keyword(s):  
Cell Wall ◽  
Current Understanding ◽  
Micronutrient Deficiencies ◽  
Developmental Defects ◽  
Essential Nutrient ◽  
Experimental Approaches ◽  
Morphological Processes ◽  
Underlying Mechanisms ◽  
Mutant Phenotypes

Abstract Deficiency of the essential nutrient boron (B) in the soil is one of the most widespread micronutrient deficiencies worldwide, leading to developmental defects in root and shoot tissues of plants, and severe yield reductions in many crops. Despite this agricultural importance, the underlying mechanisms of how B shapes plant developmental and morphological processes are still not unequivocally understood in detail. This review evaluates experimental approaches that address our current understanding of how B influences plant morphological processes by focusing on developmental defects observed under B deficiency. We assess what is known about mechanisms that control B homeostasis and specifically highlight: (i) limitations in the methodology that is used to induce B deficiency; (ii) differences between mutant phenotypes and normal plants grown under B deficiency; and (iii) recent research on analyzing interactions between B and phytohormones. Our analysis highlights the need for standardized methodology to evaluate the roles of B in the cell wall versus other parts of the cell.

scholarly journals Calcium Signaling in Vertebrate Development and Its Role in Disease

2018 ◽  
Vol 19 (11) ◽  
pp. 3390 ◽  
Author(s):  
Sudip Paudel ◽  
Regan Sindelar ◽  
Margaret Saha
Keyword(s):  
Calcium Signaling ◽  
Critical Role ◽  
Molecular Techniques ◽  
Model Organisms ◽  
Vertebrate Development ◽  
Developmental Defects ◽  
Calcium Activity ◽  
Human Genes ◽  
Underlying Mechanisms

Accumulating evidence over the past three decades suggests that altered calcium signaling during development may be a major driving force for adult pathophysiological events. Well over a hundred human genes encode proteins that are specifically dedicated to calcium homeostasis and calcium signaling, and the majority of these are expressed during embryonic development. Recent advances in molecular techniques have identified impaired calcium signaling during development due to either mutations or dysregulation of these proteins. This impaired signaling has been implicated in various human diseases ranging from cardiac malformations to epilepsy. Although the molecular basis of these and other diseases have been well studied in adult systems, the potential developmental origins of such diseases are less well characterized. In this review, we will discuss the recent evidence that examines different patterns of calcium activity during early development, as well as potential medical conditions associated with its dysregulation. Studies performed using various model organisms, including zebrafish, Xenopus, and mouse, have underscored the critical role of calcium activity in infertility, abortive pregnancy, developmental defects, and a range of diseases which manifest later in life. Understanding the underlying mechanisms by which calcium regulates these diverse developmental processes remains a challenge; however, this knowledge will potentially enable calcium signaling to be used as a therapeutic target in regenerative and personalized medicine.

Targeting emerging Mycobacterium avium infections: perspectives into pathways and antimicrobials for future interventions

2021 ◽  
Author(s):  
Rohini Mattoo
Keyword(s):  
Drug Resistance ◽  
Cell Wall ◽  
Mycobacterium Avium ◽  
Opportunistic Pathogen ◽  
Complete Eradication ◽  
Novel Therapeutics ◽  
Unique Structure ◽  
Source Of Infection ◽  
Avium Infection ◽  
Underlying Mechanisms

Mycobacterium avium is an emerging opportunistic pathogen, globally. Infections caused by M. avium are laborious to treat and could result in drug resistance. This review discusses the importance of many factors including the cell wall in M. avium pathogenesis, since this unique structure modulates the pathogen’s ability to thrive in various hosts and environmental niches including conferring resistance to killing by antimicrobials. More research efforts in future are solicited to develop novel therapeutics targeting M. avium. The complete eradication of M. avium infection in immunocompromised individuals would need a deeper understanding of the source of infection, unique underlying mechanisms and its uncharacterized pathways. This could, perhaps in future, hold the key to target and treat M. avium more effectively.

scholarly journals Twinfilin is required for actin-dependent developmental processes in Drosophila

2001 ◽  
Vol 155 (5) ◽  
pp. 787-796 ◽  
Author(s):  
Gudrun Wahlström ◽  
Maria Vartiainen ◽  
Lumi Yamamoto ◽  
Pieta K. Mattila ◽  
Pekka Lappalainen ◽  
...  
Keyword(s):  
Developmental Stages ◽  
Biological Function ◽  
Actin Monomer ◽  
Wild Type ◽  
Developmental Processes ◽  
Developmental Defects ◽  
Actin Bundles ◽  
Morphological Processes ◽  
Encoding Gene ◽  
Different Tissues

The actin cytoskeleton is essential for cellular remodeling and many developmental and morphological processes. Twinfilin is a ubiquitous actin monomer–binding protein whose biological function has remained unclear. We discovered and cloned the Drosophila twinfilin homologue, and show that this protein is ubiquitously expressed in different tissues and developmental stages. A mutation in the twf gene leads to a number of developmental defects, including aberrant bristle morphology. This results from uncontrolled polymerization of actin filaments and misorientation of actin bundles in developing bristles. In wild-type bristles, twinfilin localizes diffusively to cytoplasm and to the ends of actin bundles, and may therefore be involved in localization of actin monomers in cells. We also show that twinfilin and the ADF/cofilin encoding gene twinstar interact genetically in bristle morphogenesis. These results demonstrate that the accurate regulation of size and dynamics of the actin monomer pool by twinfilin is essential for a number of actin-dependent developmental processes in multicellular eukaryotes.

SEARCHING AND MINING VISUALLY OBSERVED PHENOTYPES OF MAIZE MUTANTS

2007 ◽  
Vol 05 (06) ◽  
pp. 1193-1213 ◽  
Author(s):  
CHI-REN SHYU ◽  
JATURON HARNSOMBURANA ◽  
JASON GREEN ◽  
ADRIAN S. BARB ◽  
TONI KAZIC ◽  
...  
Keyword(s):  
Cell Biology ◽  
Species Conservation ◽  
Genetic Maps ◽  
Cell Physiology ◽  
Complex Processes ◽  
Intimate Knowledge ◽  
Scientific Challenge ◽  
Underlying Mechanisms ◽  
Mutant Phenotypes ◽  
High Level

There are thousands of maize mutants, which are invaluable resources for plant research. Geneticists use them to study underlying mechanisms of biochemistry, cell biology, cell development, and cell physiology. To streamline the understanding of such complex processes, researchers need the most current versions of genetic and physical maps, tools with the ability to recognize novel phenotypes or classify known phenotypes, and an intimate knowledge of the biochemical processes generating physiological and phenotypic effects. They must also know how all of these factors change and differ among species, diverse alleles, germplasms, and environmental conditions. While there are robust databases, such as MaizeGDB, for some of these types of raw data, other crucial components are missing. Moreover, the management of visually observed mutant phenotypes is still in its infant stage, let alone the complex query methods that can draw upon high-level and aggregated information to answer the questions of geneticists. In this paper, we address the scientific challenge and propose to develop a robust framework for managing the knowledge of visually observed phenotypes, mining the correlation of visual characteristics with genetic maps, and discovering the knowledge relating to cross-species conservation of visual and genetic patterns. The ultimate goal of this research is to allow a geneticist to submit phenotypic and genomic information on a mutant to a knowledge base and ask, "What genes or environmental factors cause this visually observed phenotype?".

scholarly journals Regulation of sugar metabolism genes in the nitrogen-dependent susceptibility of tomato stems to Botrytis cinerea

2020 ◽  
Vol 127 (1) ◽  
pp. 143-154
Author(s):  
Nathalie Lacrampe ◽  
Félicie Lopez-Lauri ◽  
Raphaël Lugan ◽  
Sophie Colombié ◽  
Jérôme Olivares ◽  
...  
Keyword(s):  
Cell Wall ◽  
Botrytis Cinerea ◽  
Sucrose Synthase ◽  
Nitrogen Availability ◽  
Soluble Sugars ◽  
Plant Defence ◽  
Sugar Metabolism ◽  
Sugar Transporters ◽  
Expression Of Genes ◽  
Underlying Mechanisms

Abstract Background and Aims The main soluble sugars are important components of plant defence against pathogens, but the underlying mechanisms are unclear. Upon infection by Botrytis cinerea, the activation of several sugar transporters, from both plant and fungus, illustrates the struggle for carbon resources. In sink tissues, the metabolic use of the sugars mobilized in the synthesis of defence compounds or antifungal barriers is not fully understood. Methods In this study, the nitrogen-dependent variation of tomato stem susceptibility to B. cinerea was used to examine, before and throughout the course of infection, the transcriptional activity of enzymes involved in sugar metabolism. Under different nitrate nutrition regimes, the expression of genes that encode the enzymes of sugar metabolism (invertases, sucrose synthases, hexokinases, fructokinases and phosphofructokinases) was determined and sugar contents were measured before inoculation and in asymptomatic tissues surrounding the lesions after inoculation. Key Results At high nitrogen availability, decreased susceptibility was associated with the overexpression of several genes 2 d after inoculation: sucrose synthases Sl-SUS1 and Sl-SUS3, cell wall invertases Sl-LIN5 to Sl-LIN9 and some fructokinase and phosphofructokinase genes. By contrast, increased susceptibility corresponded to the early repression of several genes that encode cell wall invertase and sucrose synthase. The course of sugar contents was coherent with gene expression. Conclusions The activation of specific genes that encode sucrose synthase is required for enhanced defence. Since the overexpression of fructokinase is also associated with reduced susceptibility, it can be hypothesized that supplementary sucrose cleavage by sucrose synthases is dedicated to the production of cell wall components from UDP-glucose, or to the additional implication of fructose in the synthesis of antimicrobial compounds, or both.

scholarly journals Proprotein Convertase Furina Is Required for Heart Development in Zebrafish

2021 ◽  
Author(s):  
Qinchao Zhou ◽  
Lei Lei ◽  
Hefei Zhang ◽  
Shih-Ching Chiu ◽  
Lu Gao ◽  
...  
Keyword(s):  
Heart Development ◽  
Positional Cloning ◽  
Notch Receptor ◽  
Post Translational Modification ◽  
Proprotein Convertase ◽  
Cardiac Looping ◽  
Heart Looping ◽  
Pharyngeal Arch Arteries ◽  
Underlying Mechanisms ◽  
Mutant Phenotypes

Cardiac looping and trabeculation are key processes during cardiac chamber maturation. However, the underlying mechanisms remain incompletely understood. Here, we report the isolation, cloning, and characterization of the proprotein convertase furina from the cardiovascular mutant loft in zebrafish. loft is an ethylnitrosourea-induced mutant and has evident defects in the cardiac outflow tract, heart looping and trabeculation, the craniofacial region, and pharyngeal arch arteries. Positional cloning revealed that furina mRNA was barely detectable in loft mutants, and loft failed to complement the TALEN-induced furina mutant pku338, confirming that furina is responsible for the loft mutant phenotypes. Mechanistic studies demonstrated that Notch reporter Tg(tp1:mCherry) signals were largely eliminated in mutant hearts, while over-expression of NICD partially rescued the mutant phenotypes, probably due to the lack of Furina-mediated cleavage processing of Notch1b proteins, the only Notch receptor expressed in the heart. Together, our data suggest a potential post-translational modification of Notch1b proteins via the proprotein convertase Furina in the heart and unveil the function of the Furina-Notch1b axis in cardiac looping and trabeculation in zebrafish and possibly in other organisms.

scholarly journals Strain Degeneration in Pleurotus ostreatus: A Genotype Dependent Oxidative Stress Process Which Triggers Oxidative Stress, Cellular Detoxifying and Cell Wall Reshaping Genes

2021 ◽  
Vol 7 (10) ◽  
pp. 862
Author(s):  
Gumer Pérez ◽  
Federico Lopez-Moya ◽  
Emilia Chuina ◽  
María Ibañez-Vea ◽  
Edurne Garde ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Wall ◽  
Pleurotus Ostreatus ◽  
Constitutive Expression ◽  
Model Organism ◽  
Edible Mushroom ◽  
High Osmolarity Glycerol ◽  
Solid Media ◽  
Experimental Approaches ◽  
Molecular Aspects

Strain degeneration has been defined as a decrease or loss in the yield of important commercial traits resulting from subsequent culture, which ultimately leads to Reactive Oxygen Species (ROS) production. Pleurotus ostreatus is a lignin-producing nematophagous edible mushroom. Mycelia for mushroom production are usually maintained in subsequent culture in solid media and frequently show symptoms of strain degeneration. The dikaryotic strain P. ostreatus (DkN001) has been used in our lab as a model organism for different purposes. Hence, different tools have been developed to uncover genetic and molecular aspects of this fungus. In this work, strain degeneration was studied in a full-sib monokaryotic progeny of the DkN001 strain with fast (F) and slow (S) growth rates by using different experimental approaches (light microscopy, malondialdehyde levels, whole-genome transcriptome analysis, and chitosan effect on monokaryotic mycelia). The results obtained showed that: (i) strain degeneration in P. ostreatus is linked to oxidative stress, (ii) the oxidative stress response in monokaryons is genotype dependent, (iii) stress and detoxifying genes are highly expressed in S monokaryons with symptoms of strain degeneration, (iv) chitosan addition to F and S monokaryons uncovered the constitutive expression of both oxidative stress and cellular detoxifying genes in S monokaryon strains which suggest their adaptation to oxidative stress, and (v) the overexpression of the cell wall genes, Uap1 and Cda1, in S monokaryons with strain degeneration phenotype indicates cell wall reshaping and the activation of High Osmolarity Glycerol (HOG) and Cell Wall Integrity (CWI) pathways. These results could constitute a hallmark for mushroom producers to distinguish strain degeneration in commercial mushrooms.

scholarly journals Actomyosin Dynamics Determine the Extension and Retraction of Filopodia on Neuronal Dendrites

2016 ◽  
Author(s):  
Olena O. Marchenko ◽  
Sulagna Das ◽  
Ji Yu ◽  
Igor L. Novak ◽  
Vladimir I. Rodionov ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Actin Polymerization ◽  
Image Data ◽  
Equation Model ◽  
Retrograde Flow ◽  
Neuronal Dendrites ◽  
Substrate Adhesion ◽  
Partial Differential Equation Model ◽  
Experimental Approaches ◽  
Underlying Mechanisms

Impact StatementIn this study, using a combination of computational and experimental approaches we show that a complex dynamic behavior of dendritic filopodia that is essential for synaptogenesis is explained by an interplay among forces generated by actin retrograde flow, myosin contractility, and substrate adhesion.AbstractDendritic filopodia are actin-filled dynamic subcellular structures that sprout on neuronal dendrites during neurogenesis. The exploratory motion of the filopodia is crucial for synaptogenesis but the underlying mechanisms are poorly understood. To study the filopodial motility, we collected and analyzed image data on filopodia in cultured rat hippocampal neurons. We hypothesized that mechanical feedback among the actin retrograde flow, myosin activity and substrate adhesion gives rise to various filopodial behaviors. We have formulated a minimal one-dimensional partial differential equation model that reproduced the range of observed motility. To validate our model, we systematically manipulated experimental correlates of parameters in the model: substrate adhesion strength, actin polymerization rate, myosin contractility and the integrity of the putative microtubule-based barrier at the filopodium base. The model predicts the response of the system to each of these experimental perturbations, supporting the hypothesis that our actomyosin-driven mechanism controls dendritic filopodia dynamics.

scholarly journals Evolutionary Conservation and Essential Function of Human and Maize RNA Binding Motif Protein 48 (RBM48) in U12-Type Intron Splicing

2020 ◽  
Author(s):  
Amy E. Siebert ◽  
Jacob Corll ◽  
J. Paige Gronevelt ◽  
Laurel Levine ◽  
Linzi M. Hobbs ◽  
...  
Keyword(s):  
Rna Binding ◽  
Normal Growth ◽  
Evolutionary Conservation ◽  
Endosperm Development ◽  
Binding Motif ◽  
Intron Splicing ◽  
Rna Seq ◽  
Developmental Defects ◽  
Mutant Phenotypes ◽  
A Minor

AbstractU12-type (minor) introns are found in most multicellular eukaryotes and constitute ∼0.5% of all introns in species with a minor spliceosome required for their splicing. However, the biological relevance of U12-type introns is not well understood. It is known that mutations resulting in aberrant U12-type intron splicing cause developmental defects in both plants and animals. We recently reported that maize RNA Binding Motif Protein 48 (RBM48) is an essential splicing factor for U12-type introns. Maize rbm48 mutants display aberrant genome-wide U12-type intron splicing. This leads to severe defects in endosperm development, resulting in non-viable seeds. In this report, we use CRISPR/Cas9-mediated ablation of RBM48 in human K-562 cells to establish the evolutionary conservation of RBM48 dependent U12-type intron splicing between maize and humans. Comparative RNA-seq analysis performed on RBM48 deficient human cell lines and maize endosperm defined a subset of orthologous minor U12-type containing genes (MIGs) displaying aberrant splicing of U12-type introns in both species. Mutations in the majority of these MIGs have been reported to cause developmental defects in both plants and animals. Thus, a comparison of RNA-seq data between distantly related species containing mutations in RBM48 identifies candidate genes likely to mediate mutant phenotypes of U12-type splicing defects. Our results elucidate deeply conserved post-transcriptional processing mechanisms that are required for normal growth and development of eukaryotes with a minor spliceosome.

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