scholarly journals Muscular Development in Urechis unicinctus (Echiura, Annelida)

2020 ◽  
Vol 21 (7) ◽  
pp. 2306
Author(s):  
Yong-Hee Han ◽  
Kyoung-Bin Ryu ◽  
Brenda I. Medina Jiménez ◽  
Jung Kim ◽  
Hae-Youn Lee ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Developmental Process ◽  
Muscle Fibers ◽  
Muscle Layer ◽  
Entire Body ◽  
Urechis Unicinctus ◽  
Spatiotemporal Expression ◽  
Muscle Genes ◽  
Body Segmentation ◽  
Body Wall Muscles

Echiura is one of the most intriguing major subgroups of phylum Annelida because, unlike most other annelids, echiuran adults lack metameric body segmentation. Urechis unicinctus lives in U-shape burrows of soft sediments. Little is known about the molecular mechanisms underlying the development of U. unicinctus. Herein, we overviewed the developmental process from zygote to juvenile U. unicinctus using immunohistochemistry and F-actin staining for the nervous and muscular systems, respectively. Through F-actin staining, we found that muscle fibers began to form in the trochophore phase and that muscles for feeding were produced first. Subsequently, in the segmentation larval stage, the transversal muscle was formed in the shape of a ring in an anterior-to-posterior direction with segment formation, as well as a ventromedian muscle for the formation of a ventral nerve cord. After that, many muscle fibers were produced along the entire body and formed the worm-shaped larva. Finally, we investigated the spatiotemporal expression of Uun_st-mhc, Uun_troponin I, Uun_calponin, and Uun_twist genes found in U. unicinctus. During embryonic development, the striated and smooth muscle genes were co-expressed in the same region. However, the adult body wall muscles showed differential gene expression of each muscle layer. The results of this study will provide the basis for the understanding of muscle differentiation in Echiura.

scholarly journals Influence of layer separation on the determination of stomach smooth muscle properties

2021 ◽  
Author(s):  
Mischa Borsdorf ◽  
Markus Böl ◽  
Tobias Siebert
Keyword(s):  
Smooth Muscle ◽  
Muscle Fibers ◽  
Smooth Muscles ◽  
Muscle Layer ◽  
Uniaxial Tensile ◽  
Muscle Properties ◽  
Layer Separation ◽  
Isotonic Contractions ◽  
Longitudinal Layer

AbstractUniaxial tensile experiments are a standard method to determine the contractile properties of smooth muscles. Smooth muscle strips from organs of the urogenital and gastrointestinal tract contain multiple muscle layers with different muscle fiber orientations, which are frequently not separated for the experiments. During strip activation, these muscle fibers contract in deviant orientations from the force-measuring axis, affecting the biomechanical characteristics of the tissue strips. This study aimed to investigate the influence of muscle layer separation on the determination of smooth muscle properties. Smooth muscle strips, consisting of longitudinal and circumferential muscle layers (whole-muscle strips [WMS]), and smooth muscle strips, consisting of only the circumferential muscle layer (separated layer strips [SLS]), have been prepared from the fundus of the porcine stomach. Strips were mounted with muscle fibers of the circumferential layer inline with the force-measuring axis of the uniaxial testing setup. The force–length (FLR) and force–velocity relationships (FVR) were determined through a series of isometric and isotonic contractions, respectively. Muscle layer separation revealed no changes in the FLR. However, the SLS exhibited a higher maximal shortening velocity and a lower curvature factor than WMS. During WMS activation, the transversally oriented muscle fibers of the longitudinal layer shortened, resulting in a narrowing of this layer. Expecting volume constancy of muscle tissue, this narrowing leads to a lengthening of the longitudinal layer, which counteracted the shortening of the circumferential layer during isotonic contractions. Consequently, the shortening velocities of the WMS were decreased significantly. This effect was stronger at high shortening velocities.

scholarly journals Functional antagonism of chromatin modulators regulates epithelial-mesenchymal transition

2021 ◽  
Vol 7 (9) ◽  
pp. eabd7974
Author(s):  
Michela Serresi ◽  
Sonia Kertalli ◽  
Lifei Li ◽  
Matthias Jürgen Schmitt ◽  
Yuliia Dramaretska ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Transcriptional Control ◽  
Molecular Mechanisms ◽  
Developmental Process ◽  
Epithelial Mesenchymal Transition ◽  
Chromatin Remodelers ◽  
Mesenchymal Transition ◽  
Signature Genes ◽  
Chromatin Regulators ◽  
The Impact

Epithelial-mesenchymal transition (EMT) is a developmental process hijacked by cancer cells to modulate proliferation, migration, and stress response. Whereas kinase signaling is believed to be an EMT driver, the molecular mechanisms underlying epithelial-mesenchymal interconversion are incompletely understood. Here, we show that the impact of chromatin regulators on EMT interconversion is broader than that of kinases. By combining pharmacological modulation of EMT, synthetic genetic tracing, and CRISPR interference screens, we uncovered a minority of kinases and several chromatin remodelers, writers, and readers governing homeostatic EMT in lung cancer cells. Loss of ARID1A, DOT1L, BRD2, and ZMYND8 had nondeterministic and sometimes opposite consequences on epithelial-mesenchymal interconversion. Together with RNAPII and AP-1, these antagonistic gatekeepers control chromatin of active enhancers, including pan-cancer-EMT signature genes enabling supraclassification of anatomically diverse tumors. Thus, our data uncover general principles underlying transcriptional control of cancer cell plasticity and offer a platform to systematically explore chromatin regulators in tumor-state–specific therapy.

scholarly journals Pathways of Pathogenicity: Transcriptional Stages of Germination in the Fatal Fungal PathogenRhizopus delemar

mSphere ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Poppy C. S. Sephton-Clark ◽  
Jose F. Muñoz ◽  
Elizabeth R. Ballou ◽  
Christina A. Cuomo ◽  
Kerstin Voelz
Keyword(s):  
Molecular Mechanisms ◽  
Developmental Stages ◽  
Developmental Process ◽  
Fungal Spores ◽  
Hyphal Growth ◽  
Large Shift ◽  
Rhizopus Delemar ◽  
Content Type ◽  
Transcriptional Changes ◽  
Dormant Spore

ABSTRACTRhizopus delemaris an invasive fungal pathogen responsible for the frequently fatal disease mucormycosis. Germination, a crucial mechanism by which infectious spores ofRhizopus delemarcause disease, is a key developmental process that transforms the dormant spore state into a vegetative one. The molecular mechanisms that underpin this transformation may be key to controlling mucormycosis; however, the regulation of germination remains poorly understood. This study describes the phenotypic and transcriptional changes that take place over the course of germination. This process is characterized by four distinct stages: dormancy, isotropic swelling, germ tube emergence, and hyphal growth. Dormant spores are shown to be transcriptionally unique, expressing a subset of transcripts absent in later developmental stages. A large shift in the expression profile is prompted by the initiation of germination, with genes involved in respiration, chitin, cytoskeleton, and actin regulation appearing to be important for this transition. A period of transcriptional consistency can be seen throughout isotropic swelling, before the transcriptional landscape shifts again at the onset of hyphal growth. This study provides a greater understanding of the regulation of germination and highlights processes involved in transformingRhizopus delemarfrom a single-cellular to multicellular organism.IMPORTANCEGermination is key to the growth of many organisms, including fungal spores. Mucormycete spores exist abundantly within the environment and germinate to form hyphae. These spores are capable of infecting immunocompromised individuals, causing the disease mucormycosis. Germination from spore to hyphae within patients leads to angioinvasion, tissue necrosis, and often fatal infections. This study advances our understanding of how spore germination occurs in the mucormycetes, identifying processes we may be able to inhibit to help prevent or treat mucormycosis.

scholarly journals Molecular Mechanisms Involved in the Multicellular Growth of Ustilaginomycetes

2020 ◽  
Vol 8 (7) ◽  
pp. 1072
Author(s):  
Domingo Martínez-Soto ◽  
Lucila Ortiz-Castellanos ◽  
Mariana Robledo-Briones ◽  
Claudia Geraldine León-Ramírez
Keyword(s):  
Molecular Mechanisms ◽  
Developmental Process ◽  
Culture Media ◽  
Morphological Plasticity ◽  
Model Organisms ◽  
Fruiting Bodies ◽  
Daughter Cells ◽  
Plant Infection ◽  
Polarized Cell Growth ◽  
Unicellular Organisms

Multicellularity is defined as the developmental process by which unicellular organisms became pluricellular during the evolution of complex organisms on Earth. This process requires the convergence of genetic, ecological, and environmental factors. In fungi, mycelial and pseudomycelium growth, snowflake phenotype (where daughter cells remain attached to their stem cells after mitosis), and fruiting bodies have been described as models of multicellular structures. Ustilaginomycetes are Basidiomycota fungi, many of which are pathogens of economically important plant species. These fungi usually grow unicellularly as yeasts (sporidia), but also as simple multicellular forms, such as pseudomycelium, multicellular clusters, or mycelium during plant infection and under different environmental conditions: Nitrogen starvation, nutrient starvation, acid culture media, or with fatty acids as a carbon source. Even under specific conditions, Ustilago maydis can form basidiocarps or fruiting bodies that are complex multicellular structures. These fungi conserve an important set of genes and molecular mechanisms involved in their multicellular growth. In this review, we will discuss in-depth the signaling pathways, epigenetic regulation, required polyamines, cell wall synthesis/degradation, polarized cell growth, and other cellular-genetic processes involved in the different types of Ustilaginomycetes multicellular growth. Finally, considering their short life cycle, easy handling in the laboratory and great morphological plasticity, Ustilaginomycetes can be considered as model organisms for studying fungal multicellularity.

Linking Organelle Remodeling with the Erythroid Cell Genetic Network

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 367-367
Author(s):  
Yoon-A Kang ◽  
Jonathan N Ouellette ◽  
Genís Campreciós ◽  
Saghi Ghaffari ◽  
Emery H Bresnick
Keyword(s):  
Input Signal ◽  
Molecular Mechanisms ◽  
Developmental Process ◽  
Conflicts Of Interest ◽  
Network Motif ◽  
Genetic Network ◽  
Genetic Networks ◽  
Cell Maturation ◽  
Erythroid Cell ◽  
Crucial Step

Abstract Abstract 367 Developmental processes such as hematopoiesis are regulated by complex genetic networks, which can be deconstructed into regulatory modules termed network motifs. Although considerable progress has been made in defining genetic networks that control hematopoiesis, many questions remain regarding how such networks are established and maintained. We provide evidence for an important network motif involving the master regulator of erythropoiesis GATA-1 and the forkhead transcription factor FoxO3, which instigates autophagy as an important component of the erythroid cell genetic network. Autophagy mediates organelle remodeling, including the consumption of mitochondria, as a critical developmental process and as a cellular quality control mechanism. Whereas autophagy has been analyzed extensively under stress conditions, mechanisms that instigate and regulate autophagy in specialized cell and tissue types are much less understood. In a genetic complementation assay in G1E-ER-GATA-1 cells, ER-GATA-1 directly activated transcription of essential autophagy genes, including the gene encoding Microtubule Associated Protein 1 Light Chain 3B (LC3B). GATA-1-mediated LC3B induction was associated with increased LC3B-positive autophagosomes, based on immunofluorescence studies. We developed transmission electron microscopy/immunogold labeling assays, which uniquely allow one to mechanistically dissect how a single regulatory factor (GATA-1) orchestrates organelle remodeling as a crucial step in terminal maturation. This analysis provided evidence that GATA-1 induction of LC3B is linked to increased autophagosome/autophagolysosome numbers per cell and to increased autophagosome/autophagolysosome size. As these organelles mediate mitochondrial clearance as a crucial step in erythropoiesis, we investigated the underlying molecular mechanisms. We demonstrated that GATA-1 directly activates autophagy genes and induces FoxO3, another direct activator of autophagy genes. This dual regulatory mechanism constitutes a type 1 coherent feed-forward loop, a network motif that can buffer input signal noise (GATA-1 level/activity), thus preventing a premature output (autophagy). In principle, a sustained input signal translates into an irreversible autophagy output. GATA-1 induced FoxO3 protein 6.7 fold (p < 0.001) and FoxO3 chromatin occupancy (3 fold, p < 0.0001). FoxO3 occupied chromatin adjacent to the GATA-1 occupancy site at select GATA-1 target gene loci. siRNA-mediated knockdown of FoxO3 in G1E-ER-GATA-1 cells reduced the capacity of GATA-1 to regulate select autophagy genes. A similar impact of FoxO3 loss on these genes was detected with bone marrow-derived erythroblasts from FoxO3-nullizygous mice. Our results establish a novel genetic mechanism that instigates cell type-specific autophagy as an important step in erythroid cell maturation. These studies support a model in which GATA-1-dependent autophagy is a crucial driving force in erythropoiesis, and specific molecular steps in organelle remodeling are inextricably linked to the erythroid cell genetic network. Perturbation of this mechanism may lead to the accumulation of functionally defective intermediates in autophagosome/autophagolysosome assembly with ensuing erythroid cell maturation defects and pathologies. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Skeletal myosin heavy chain function in cultured lung myofibroblasts

2003 ◽  
Vol 163 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Nancy A. Rice ◽  
Leslie A. Leinwand
Keyword(s):  
Skeletal Muscle ◽  
Promoter Activity ◽  
Molecular Mechanisms ◽  
Smooth Muscle Actin ◽  
Myogenic Regulatory Factor ◽  
Skeletal Muscle Myosin ◽  
Heavy Chains ◽  
Skeletal Myosin ◽  
Muscle Genes ◽  
Muscle Myosin

Myofibroblasts are unique contractile cells with both muscle and nonmuscle properties. Typically myofibroblasts are identified by the expression of α smooth muscle actin (ASMA); however some myofibroblasts also express sarcomeric proteins. In this study, we show that pulmonary myofibroblasts express three of the eight known sarcomeric myosin heavy chains (MyHCs) (IIa, IId, and embryonic) and that skeletal muscle myosin enzymatic activity is required for pulmonary myofibroblast contractility. Furthermore, inhibition of skeletal myosin activity and myofibroblast contraction results in a decrease in both ASMA and skeletal MyHC promoter activity and ASMA protein expression, suggesting a potential coupling of skeletal myosin activity and ASMA expression in myofibroblast differentiation. To understand the molecular mechanisms whereby skeletal muscle genes are regulated in myofibroblasts, we have found that members of the myogenic regulatory factor family of transcription factors and Ca2+-regulated pathways are involved in skeletal MyHC promoter activity. Interestingly, the regulation of skeletal myosin expression in myofibroblasts is distinct from that observed in muscle cells and suggests that cell context is important in its control.

scholarly journals Role of proinflammatory cytokines and growth factors in skeletal muscle regeneration

2016 ◽  
Vol 72 (8) ◽  
pp. 472-478
Author(s):  
Marta Milewska ◽  
Katarzyna Grzelkowska-Kowalczyk
Keyword(s):  
Skeletal Muscle ◽  
Growth Factors ◽  
Proinflammatory Cytokines ◽  
Muscle Regeneration ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Muscle Fibers ◽  
Skeletal Muscle Regeneration ◽  
Functional Efficiency

Skeletal muscle healing after injury can be divided into three distinct but overlapping phases. The destruction phase is characterized by rupture followed by necrosis of muscle fibers, formation of hematoma and inflammatory reaction. During the repair phase a necrotic tissue is phagocyted by macrophages, muscle fibers are regenerating and connective tissue scars are formed. The remodeling phase concerns the period when regenerating muscle fibers mature, scar contraction and reorganization occurs and the muscle recovers its functional efficiency. Proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and growth factors (FGF, IGF, TGF-β, HGF) play a critical role in all phases of muscle repair. Moreover, chemokines expressed at early stages of myogenesis can regulate the survival and proliferation of myoblasts. Chemokines expressed in vivo in muscle cells can directly influence myogenesis, but can also act in a paracrine manner by recruiting the immune cells (macrophages) to injured skeletal muscles, which is crucial for the regeneration process. Identification of molecules regulating myogenesis, like cytokines, chemokines and growth factors, contributes to the exploration of molecular mechanisms that can improve muscle regeneration after injury, diseases, surgery and increase the effectiveness of cell transplantation.

scholarly journals Sophisticated Gene Regulation for a Complex Physiological System: The Role of Non-coding RNAs in Photoreceptor Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Sabrina Carrella ◽  
Sandro Banfi ◽  
Marianthi Karali
Keyword(s):  
Molecular Mechanisms ◽  
Developmental Process ◽  
Photoreceptor Cells ◽  
Sensory Transduction ◽  
Circular Rnas ◽  
Therapeutic Implications ◽  
Physiological Processes ◽  
Non Coding Rnas ◽  
And Function

Photoreceptors (PRs) are specialized neuroepithelial cells of the retina responsible for sensory transduction of light stimuli. In the highly structured vertebrate retina, PRs have a highly polarized modular structure to accommodate the demanding processes of phototransduction and the visual cycle. Because of their function, PRs are exposed to continuous cellular stress. PRs are therefore under pressure to maintain their function in defiance of constant environmental perturbation, besides being part of a highly sophisticated developmental process. All this translates into the need for tightly regulated and responsive molecular mechanisms that can reinforce transcriptional programs. It is commonly accepted that regulatory non-coding RNAs (ncRNAs), and in particular microRNAs (miRNAs), are not only involved but indeed central in conferring robustness and accuracy to developmental and physiological processes. Here we integrate recent findings on the role of regulatory ncRNAs (e.g., miRNAs, lncRNAs, circular RNAs, and antisense RNAs), and of their contribution to PR pathophysiology. We also outline the therapeutic implications of translational studies that harness ncRNAs to prevent PR degeneration and promote their survival and function.

scholarly journals Optogenetic regulation of embryo implantation in mice using photoactivatable CRISPR-Cas9

2020 ◽  
Vol 117 (46) ◽  
pp. 28579-28581
Author(s):  
Tomoka Takao ◽  
Moritoshi Sato ◽  
Tetsuo Maruyama
Keyword(s):  
Leukemia Inhibitory Factor ◽  
Gene Editing ◽  
Therapeutic Strategy ◽  
Molecular Mechanisms ◽  
Light Emitting Diode ◽  
Embryo Implantation ◽  
Light Emitting ◽  
Spatiotemporal Expression ◽  
Fertilized Egg

Embryo implantation is achieved upon successful interaction between a fertilized egg and receptive endometrium and is mediated by spatiotemporal expression of implantation-associated molecules including leukemia inhibitory factor (LIF). Here we demonstrate, in mice, that LIF knockdown via a photoactivatable CRISPR-Cas9 gene editing system and illumination with a light-emitting diode can spatiotemporally disrupt fertility. This system enables dissection of spatiotemporal molecular mechanisms associated with embryo implantation and provides a therapeutic strategy for temporal control of reproductive functions in vivo.

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