scholarly journals Two chemically distinct root lignin barriers control solute and water balance

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Guilhem Reyt ◽  
Priya Ramakrishna ◽  
Isai Salas-González ◽  
Satoshi Fujita ◽  
Ashley Love ◽  
...  
Keyword(s):  
Critical Role ◽  
Phenylpropanoid Pathway ◽  
Cellular Functions ◽  
Casparian Strip ◽  
Transcriptional Reprogramming ◽  
Exogenous Cues ◽  
Endodermal Cells ◽  
Complex Polymer ◽  
Nutrient Homeostasis ◽  
Lignin Deposition

AbstractLignin is a complex polymer deposited in the cell wall of specialised plant cells, where it provides essential cellular functions. Plants coordinate timing, location, abundance and composition of lignin deposition in response to endogenous and exogenous cues. In roots, a fine band of lignin, the Casparian strip encircles endodermal cells. This forms an extracellular barrier to solutes and water and plays a critical role in maintaining nutrient homeostasis. A signalling pathway senses the integrity of this diffusion barrier and can induce over-lignification to compensate for barrier defects. Here, we report that activation of this endodermal sensing mechanism triggers a transcriptional reprogramming strongly inducing the phenylpropanoid pathway and immune signaling. This leads to deposition of compensatory lignin that is chemically distinct from Casparian strip lignin. We also report that a complete loss of endodermal lignification drastically impacts mineral nutrients homeostasis and plant growth.

scholarly journals Schengen-pathway controls spatially separated and chemically distinct lignin deposition in the endodermis

2020 ◽  
Author(s):  
Guilhem Reyt ◽  
Priya Ramakrishna ◽  
Isai Salas-González ◽  
Satoshi Fujita ◽  
Ashley Love ◽  
...  
Keyword(s):  
Critical Role ◽  
Phenylpropanoid Pathway ◽  
Cellular Functions ◽  
Casparian Strip ◽  
Transcriptional Reprogramming ◽  
Exogenous Cues ◽  
Endodermal Cells ◽  
Complex Polymer ◽  
Nutrient Homeostasis ◽  
Lignin Deposition

ABSTRACTLignin is a complex polymer precisely deposited in the cell wall of specialised plant cells, where it provides essential cellular functions. Plants coordinate timing, location, abundance and composition of lignin deposition in response to endogenous and exogenous cues. In roots, a fine band of lignin, the Casparian strip encircles endodermal cells. This forms an extracellular barrier to solutes and water and plays a critical role in maintaining nutrient homeostasis. A signalling pathway senses the integrity of this diffusion barrier and can induce over-lignification to compensate for barrier defects. Here, we report that activation of this endodermal sensing mechanism triggers a transcriptional reprogramming strongly inducing the phenylpropanoid pathway and immune signaling. This leads to deposition of compensatory lignin that is chemically distinct from Casparian strip lignin. We also report that a complete loss of endodermal lignification drastically impacts mineral nutrients homeostasis and plant growth.

scholarly journals Uclacyanin proteins are required for lignified nanodomain formation within Casparian strips

2020 ◽  
Author(s):  
Guilhem Reyt ◽  
Zhenfei Chao ◽  
Paulina Flis ◽  
Gabriel Castrillo ◽  
Dai-Yin Chao ◽  
...  
Keyword(s):  
Vascular Plants ◽  
Vascular System ◽  
Critical Role ◽  
Mineral Nutrient ◽  
Normal Plant ◽  
Loss Of Function ◽  
Free Diffusion ◽  
Casparian Strips ◽  
Endodermal Cells ◽  
Nutrient Homeostasis

AbstractCasparian strips (CS) are cell wall modifications of vascular plants restricting extracellular free diffusion into and out the vascular system. This barrier plays a critical role in controlling the acquisition of nutrients and water necessary for normal plant development. CS are formed by the precise deposition of a band of lignin approximately 2 μm wide and 150 nm thick spanning the apoplastic space between adjacent endodermal cells. Here, we identified a copper-containing protein, Uclacyanin1 (UCC1) that is sub-compartmentalised within the CS. UCC1 forms a central CS nanodomain in comparison with other CS-located proteins that are found to be mainly accumulated at the periphery of the CS. We found that loss-of-function of two uclacyanins (UCC1 and UCC2) reduces lignification specifically in this central CS nanodomain, revealing a nano-compartmentalised machinery for lignin polymerisation. This lack of lignification leads to increased endodermal permeability, and consequently to a loss of mineral nutrient homeostasis.

Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2

2008 ◽  
Vol 294 (6) ◽  
pp. C1521-C1530 ◽  
Author(s):  
Shuji Kondo ◽  
Yixin Tang ◽  
Elizabeth A. Scheef ◽  
Nader Sheibani ◽  
Christine M. Sorenson
Keyword(s):  
Cell Migration ◽  
Vascular System ◽  
Ex Vivo ◽  
Vascular Development ◽  
Critical Role ◽  
Endothelial Cell Migration ◽  
Cellular Functions ◽  
Capillary Morphogenesis ◽  
Angiogenesis Assay ◽  
Ischemic Retinopathy

Apoptosis plays a critical role during development and in the maintenance of the vascular system. B-cell leukemia lymphoma 2 (bcl-2) protects endothelial cells (EC) from apoptosis in response to a variety of stimuli. Previous work from this laboratory demonstrated attenuation of postnatal retinal vascular development and retinal neovascularization during oxygen-induced ischemic retinopathy in bcl-2-deficient (bcl-2−/−) mice. To gain further insight into the function of bcl-2 in the endothelium, we isolated retinal EC from bcl-2+/+ and bcl-2−/− mice. Retinal EC lacking bcl-2 demonstrated reduced cell migration, tenascin-C expression, and adhesion to vitronectin and fibronectin. The bcl-2−/− retinal EC also failed to undergo capillary morphogenesis in Matrigel. In addition, using an ex vivo angiogenesis assay, we observed reduced sprouting from aortic rings grown in culture from bcl-2−/− mice compared with bcl-2+/+ mice. Furthermore, reexpression of bcl-2 was sufficient to restore migration and capillary morphogenesis defects observed in bcl-2−/− retinal EC. Mechanistically, bcl-2−/− cells expressed significantly less endothelial nitric oxide synthase, an important downstream effecter of proangiogenic signaling. This may be attributed to increased oxidative stress in the absence of bcl-2. In fact, incubation of retinal EC or aortic rings from bcl-2−/− mice with the antioxidant N-acetylcysteine rescued their capillary morphogenesis and sprouting defects. Thus, bcl-2-mediated cellular functions play important roles not only in survival but also in proangiogenic phenotype of EC with a significant impact on vascular development and angiogenesis.

scholarly journals Regulation of intracellular membrane trafficking and cell dynamics by syntaxin-6

2012 ◽  
Vol 32 (4) ◽  
pp. 383-391 ◽  
Author(s):  
Jae-Joon Jung ◽  
Shivangi M. Inamdar ◽  
Ajit Tiwari ◽  
Amit Choudhury
Keyword(s):  
Membrane Trafficking ◽  
Critical Role ◽  
Cell Types ◽  
Intracellular Membrane ◽  
Cellular Functions ◽  
Cell Dynamics ◽  
Transport Pathways ◽  
Protein Receptor ◽  
Secretory Transport ◽  
Target Membrane

Intracellular membrane trafficking along endocytic and secretory transport pathways plays a critical role in diverse cellular functions including both developmental and pathological processes. Briefly, proteins and lipids destined for transport to distinct locations are collectively assembled into vesicles and delivered to their target site by vesicular fusion. SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein receptor) proteins are required for these events, during which v-SNAREs (vesicle SNAREs) interact with t-SNAREs (target SNAREs) to allow transfer of cargo from donor vesicle to target membrane. Recently, the t-SNARE family member, syntaxin-6, has been shown to play an important role in the transport of proteins that are key to diverse cellular dynamic processes. In this paper, we briefly discuss the specific role of SNAREs in various mammalian cell types and comprehensively review the various roles of the Golgi- and endosome-localized t-SNARE, syntaxin-6, in membrane trafficking during physiological as well as pathological conditions.

scholarly journals Uridine Metabolism and Its Role in Glucose, Lipid, and Amino Acid Homeostasis

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yumei Zhang ◽  
Songge Guo ◽  
Chunyan Xie ◽  
Jun Fang
Keyword(s):  
Amino Acid ◽  
Acid Metabolism ◽  
De Novo ◽  
Feeding Habits ◽  
Critical Role ◽  
Atp Depletion ◽  
Cellular Functions ◽  
Drug Induced ◽  
Three Stages ◽  
Amino Acid Homeostasis

Pyrimidine nucleoside uridine plays a critical role in maintaining cellular function and energy metabolism. In addition to its role in nucleoside synthesis, uridine and its derivatives contribute to reduction of cytotoxicity and suppression of drug-induced hepatic steatosis. Uridine is mostly present in blood and cerebrospinal fluid, where it contributes to the maintenance of basic cellular functions affected by UPase enzyme activity, feeding habits, and ATP depletion. Uridine metabolism depends on three stages: de novo synthesis, salvage synthesis pathway and catabolism, and homeostasis, which is tightly relating to glucose homeostasis and lipid and amino acid metabolism. This review is devoted to uridine metabolism and its role in glucose, lipid, and amino acid homeostasis.

scholarly journals Autophagy in the endocrine glands

2014 ◽  
Vol 52 (2) ◽  
pp. R151-R163 ◽  
Author(s):  
Andrea Weckman ◽  
Antonio Di Ieva ◽  
Fabio Rotondo ◽  
Luis V Syro ◽  
Leon D Ortiz ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Secretory Granules ◽  
Critical Role ◽  
Endocrine System ◽  
Specific Form ◽  
The Body ◽  
Endocrine Glands ◽  
Cellular Functions ◽  
Endocrine Diseases ◽  
Wide Range

Autophagy is an important cellular process involving the degradation of intracellular components. Its regulation is complex and while there are many methods available, there is currently no single effective way of detecting and monitoring autophagy. It has several cellular functions that are conserved throughout the body, as well as a variety of different physiological roles depending on the context of its occurrence in the body. Autophagy is also involved in the pathology of a wide range of diseases. Within the endocrine system, autophagy has both its traditional conserved functions and specific functions. In the endocrine glands, autophagy plays a critical role in controlling intracellular hormone levels. In peptide-secreting cells of glands such as the pituitary gland, crinophagy, a specific form of autophagy, targets the secretory granules to control the levels of stored hormone. In steroid-secreting cells of glands such as the testes and adrenal gland, autophagy targets the steroid-producing organelles. The dysregulation of autophagy in the endocrine glands leads to several different endocrine diseases such as diabetes and infertility. This review aims to clarify the known roles of autophagy in the physiology of the endocrine system, as well as in various endocrine diseases.

Probable sites for passive movement of ions across the endodermis

1971 ◽  
Vol 49 (1) ◽  
pp. 35-38 ◽  
Author(s):  
E. B. Dumbroff ◽  
D. R. Peirson
Keyword(s):  
Fluorescence Microscopy ◽  
Mass Flow ◽  
Lateral Root ◽  
Lateral Roots ◽  
Passive Movement ◽  
General Picture ◽  
Effective Barrier ◽  
Casparian Strip ◽  
Endodermal Cells ◽  
The Relationship

The endodermis, with its associated Casparian strip, is generally believed to act as an effective barrier to the passive movement of ions from the cortex to the xylem in young roots. However, several workers have suggested that the functional integrity of the endodermis might be somewhat impaired with the emergence of branch roots from the pericycle, thus providing pathways for the mass flow of water and ions into the stele. The present work was undertaken to examine the validity of this hypothesis.Sections of lateral roots embedded in glycol methacrylate were stained and examined by fluorescence microscopy, and a general picture of the relationship between branch root development and concomitant changes in the endodermis emerged. The endodermal cells of the parent root were found to maintain a continuous, unbroken, suberized layer over the surface of a very young lateral root, but with continued elongation there is a period when formation of the Casparian strip lags behind division of endodermal cells. It appears likely that, at this stage, water and ions can enter the stele of the parent root by mass flow.

scholarly journals Modulation of Cell Wall Structure and Antimicrobial Susceptibility by a Staphylococcus aureus Eukaryote-Like Serine/Threonine Kinase and Phosphatase

2009 ◽  
Vol 77 (4) ◽  
pp. 1406-1416 ◽  
Author(s):  
Amanda M. Beltramini ◽  
Chitrangada D. Mukhopadhyay ◽  
Vijay Pancholi
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Gene Knockout ◽  
Critical Role ◽  
Cell Wall Structure ◽  
Wall Structure ◽  
Cellular Functions ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Irregular Cell

ABSTRACT It is well established that prokaryotes and eukaryotes alike utilize phosphotransfer to regulate cellular functions. One method by which this occurs is via eukaryote-like serine/threonine kinase (ESTK)- and phosphatase (ESTP)-regulated pathways. The role of these enzymes in Staphylococcus aureus has not yet been examined. This resilient organism is a common cause of hospital-acquired and community-associated infections, infecting immunocompromised and immunocompetent hosts alike. In this study, we have characterized a major functional ESTK (STK) and ESTP (STP) in S. aureus and found them to be critical modulators of cell wall structure and susceptibility to cell wall-acting β-lactam antibiotics. By utilizing gene knockout strategies, we created S. aureus N315 mutants lacking STP and/or STK. The strain lacking both STP and STK displayed notable cell division defects, including multiple and incomplete septa, bulging, and irregular cell size, as observed by transmission electron microscopy. Mutants lacking STP alone displayed thickened cell walls and increased resistance to the peptidoglycan-targeting glycylglycine endopeptidase lysostaphin, compared to the wild type. Additionally, mutant strains lacking STK or both STK and STP displayed increased sensitivity to cell wall-acting cephalosporin and carbapenem antibiotics. Together, these results indicate that S. aureus STK- and STP-mediated reversible phosphorylation reactions play a critical role in proper cell wall architecture, and thus the modulation of antimicrobial resistance, in S. aureus.

Radial widening of the Casparian strip follows induced radial expansion of endodermal cells

Planta ◽  
2001 ◽  
Vol 213 (3) ◽  
pp. 474-477 ◽  
Author(s):  
Masaki Yokoyama ◽  
Ichirou Karahara
Keyword(s):  
Radial Expansion ◽  
Casparian Strip ◽  
Endodermal Cells

scholarly journals A critical role for Apc in hematopoietic stem and progenitor cell survival

2008 ◽  
Vol 205 (9) ◽  
pp. 2163-2175 ◽  
Author(s):  
Zhijian Qian ◽  
Lina Chen ◽  
Anthony A. Fernald ◽  
Bart O. Williams ◽  
Michelle M. Le Beau
Keyword(s):  
Chromosome Segregation ◽  
Bone Marrow Failure ◽  
Critical Role ◽  
Cellular Functions ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem ◽  
Myeloid Progenitor ◽  
Cell Cycle Entry ◽  
Genes Encoding

The adenomatous polyposis coli (Apc) tumor suppressor is involved in the initiation and progression of colorectal cancer via regulation of the Wnt signaling cascade. In addition, Apc plays an important role in multiple cellular functions, including cell migration and adhesion, spindle assembly, and chromosome segregation. However, its role during adult hematopoiesis is unknown. We show that conditional inactivation of Apc in vivo dramatically increases apoptosis and enhances cell cycle entry of hematopoietic stem cells (HSCs)/ hematopoietic progenitor cells (HPCs), leading to their rapid disappearance and bone marrow failure. The defect in HSCs/HPCs caused by Apc ablation is cell autonomous. In addition, we found that loss of Apc leads to exhaustion of the myeloid progenitor pool (common myeloid progenitor, granulocyte-monocyte progenitor, and megakaryocyte-erythroid progenitor), as well as the lymphoid-primed multipotent progenitor pool. Down-regulation of the genes encoding Cdkn1a, Cdkn1b, and Mcl1 occurs after acute Apc excision in candidate HSC populations. Together, our data demonstrate that Apc is essential for HSC and HPC maintenance and survival.

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