scholarly journals Cell surface and intracellular auxin signalling for H+-fluxes in root growth

2021 ◽  
Author(s):  
Lanxin Li ◽  
Inge Verstraeten ◽  
Mark Roosjen ◽  
Koji Takahashi ◽  
Lesia Rodriguez ◽  
...  
Keyword(s):  
Cell Surface ◽  
Root Growth ◽  
Growth Regulation ◽  
Cellular Mechanism ◽  
Signalling Pathways ◽  
Soil Environment ◽  
Growth Modulation ◽  
Auxin Signalling ◽  
Simultaneous Activation ◽  
Apoplast Acidification

Abstract Growth regulation tailors plant development to its environment. A showcase is response to gravity, where shoots bend up and roots down1. This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots, while inhibiting it in roots via a yet unknown cellular mechanism2. Here, by combining microfluidics, live imaging, genetic engineering and phospho-proteomics in Arabidopsis thaliana, we advance our understanding how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on the rapid regulation of the apoplastic pH, a causative growth determinant. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H+-ATPases for apoplast acidification, while intracellular canonical auxin signalling promotes net cellular H+-influx, causing apoplast alkalinisation. The simultaneous activation of these two counteracting mechanisms poises the root for a rapid, fine-tuned growth modulation while navigating complex soil environment.

scholarly journals Antagonistic cell surface and intracellular auxin signalling regulate plasma membrane H+-fluxes for root growth

2021 ◽  
Author(s):  
Lanxin Li ◽  
Inge Verstraeten ◽  
Mark Roosjen ◽  
Koji Takahashi ◽  
Lesia Rodriguez ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cell Surface ◽  
Root Growth ◽  
Growth Regulation ◽  
Signalling Pathways ◽  
Soil Environment ◽  
Growth Modulation ◽  
Auxin Signalling ◽  
Simultaneous Activation ◽  
Apoplast Acidification

Abstract Growth regulation tailors plant development to its environment. A showcase is response to gravity, where shoots bend up and roots down1. This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots, while inhibiting it in roots via a yet unknown cellular mechanism2. Here, by combining microfluidics, live imaging, genetic engineering and phospho-proteomics in Arabidopsis thaliana, we advance our understanding how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on the rapid regulation of the apoplastic pH, a causative growth determinant. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H+-ATPases for apoplast acidification, while intracellular canonical auxin signalling promotes net cellular H+-influx, causing apoplast alkalinisation. The simultaneous activation of these two counteracting mechanisms poises the root for a rapid, fine-tuned growth modulation while navigating complex soil environment.

scholarly journals Antagonistic cell surface and intracellular auxin signalling regulate plasma membrane H -fluxes for root growth

2021 ◽  
Author(s):  
Lanxin Li ◽  
Inge Verstraeten ◽  
Mark Roosjen ◽  
Koji Takahashi ◽  
Lesia Rodriguez ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cell Surface ◽  
Root Growth ◽  
Growth Regulation ◽  
Growth Modulation ◽  
Auxin Signalling ◽  
Direct Growth ◽  
Simultaneous Activation ◽  
Growth Adaptation ◽  
Apoplast Acidification

Abstract Growth regulation tailors plant development to its environment. A showcase is growth adaptation to gravity, where shoots bend up and roots down. This paradox is based on different responses to the phytohormone auxin, which promotes cell expansion in shoots, while inhibiting it in roots via a yet unknown cellular mechanism. Here, by combining microfluidics, live imaging, genetic engineering and phospho-proteomics in Arabidopsis thaliana, we reveal how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on the rapid regulation of the apoplastic pH, which is the direct growth-determining mechanism. Cell surface-based TRANSMEMBRANE KINASE 1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H+-ATPases for apoplast acidification, while intracellular TIR1/AFB-mediated signalling triggers net cellular H+-influx, causing apoplast alkalinisation. The simultaneous activation of these two counteracting mechanisms poises the root for a rapid, fine-tuned growth modulation to subtle changes in the environment.

scholarly journals Cell surface and intracellular auxin signalling for H+ fluxes in root growth

Nature ◽  
2021 ◽  
Author(s):  
Lanxin Li ◽  
Inge Verstraeten ◽  
Mark Roosjen ◽  
Koji Takahashi ◽  
Lesia Rodriguez ◽  
...  
Keyword(s):  
Cell Surface ◽  
Root Growth ◽  
Auxin Signalling

scholarly journals The Arabidopsis Root Tip (Phospho)Proteomes at Growth-Promoting versus Growth-Repressing Conditions Reveal Novel Root Growth Regulators

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1665
Author(s):  
Natalia Nikonorova ◽  
Evan Murphy ◽  
Cassio Flavio Fonseca de Lima ◽  
Shanshuo Zhu ◽  
Brigitte van de Cotte ◽  
...  
Keyword(s):  
Cell Wall ◽  
Root Growth ◽  
Growth Regulators ◽  
Growth Regulation ◽  
Phosphorylation Site ◽  
Primary Root ◽  
Root Tip ◽  
Arabidopsis Root ◽  
Growth Promoting ◽  
The Impact

Auxin plays a dual role in growth regulation and, depending on the tissue and concentration of the hormone, it can either promote or inhibit division and expansion processes in plants. Recent studies have revealed that, beyond transcriptional reprogramming, alternative auxin-controlled mechanisms regulate root growth. Here, we explored the impact of different concentrations of the synthetic auxin NAA that establish growth-promoting and -repressing conditions on the root tip proteome and phosphoproteome, generating a unique resource. From the phosphoproteome data, we pinpointed (novel) growth regulators, such as the RALF34-THE1 module. Our results, together with previously published studies, suggest that auxin, H+-ATPases, cell wall modifications and cell wall sensing receptor-like kinases are tightly embedded in a pathway regulating cell elongation. Furthermore, our study assigned a novel role to MKK2 as a regulator of primary root growth and a (potential) regulator of auxin biosynthesis and signalling, and suggests the importance of the MKK2 Thr31 phosphorylation site for growth regulation in the Arabidopsis root tip.

Cell surface components and growth regulation in cultivated arterial smooth muscle cells

1983 ◽  
Vol 64 (1) ◽  
pp. 107-121
Author(s):  
J. Nilsson ◽  
T. Ksiazek ◽  
J. Thyberg ◽  
A. Wasteson
Keyword(s):  
Smooth Muscle ◽  
Sialic Acid ◽  
Cell Surface ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Growth Regulation ◽  
Heparan Sulphate ◽  
Carboxyl Groups ◽  
Anionic Sites ◽  
Arterial Smooth Muscle Cells

The surface of rat arterial smooth muscle cells was characterized with respect to some of its chemical and functional properties. The effects of selective enzymic degradations (hyaluronidase, chondroitinases, heparitinase or neuraminidase) on [35S]sulphate-prelabelled cells and on binding sites for cationized ferritin (CF) were examined to assess the presence and relative importance of individual species of macromolecules on the cell surface. The results indicate that about half of the strongly anionic sites on the cell surface (binding CF at pH 2.0) could be ascribed to sulphate groups of glycosaminoglycans and about half to carboxyl groups of sialic acid residues in glycoproteins and/or glycolipids. Weaker anionic sites (binding CF at pH 7.0) largely originated from carboxyl groups of glycosaminoglycans. Chondroitin sulphate and heparan sulphate were the main glycosaminoglycans. The surface of cells from young animals showed a higher glycosaminoglycan and a lower sialic acid content than that of cells from adult animals. Continuous treatment of the cultures with neuraminidase stimulated serum-induced initiation of DNA synthesis, while treatment with hyaluronidase or heparitinase inhibited it. Addition of hyaluronic acid, heparin or heparan sulphate to the culture medium inhibited initiation of DNA synthesis as well as cell proliferation. The effect was more marked in cultures of cells from young animals than from adults, although the latter cells were found to grow at a higher rate and to higher densities. These results suggest a role for cell-surface and pericellular glycoconjugates in growth regulation. A possible mechanism of action is that these molecules, due to their anionic charge or by steric exclusion, interfere with the binding of platelet-derived growth factor, a highly cationic polypeptide, to its cell-surface receptor.

Intracellular signalling

2020 ◽  
pp. 256-265
Author(s):  
R. Andres Floto
Keyword(s):  
Signal Transduction ◽  
Plasma Membrane ◽  
Cell Surface ◽  
Intracellular Signalling ◽  
Signalling Pathways ◽  
Molecular Processes ◽  
Surface Receptors ◽  
Intracellular Signalling Pathways ◽  
Transmission Of Information ◽  
Effective Transmission

This chapter outlines the general principles of intracellular signalling. Focusing on cell surface receptors, the requirements for effective transmission of information across the plasma membrane are outlined. The principal mechanisms utilized in mammalian signal transduction are described. For each, the pathological consequences of aberrant signalling and means by which pathways can be pharmacologically targeted are described in molecular terms. Intracellular signalling pathways permit the transmission and integration of information within cells. Mammalian receptor signalling relies on only a small number of distinct molecular processes which interact to determine cellular responses. Rapid advances in our knowledge of the mechanisms of intracellular signalling has greatly increased understanding of how cells function physiologically, how they malfunction pathologically, and how their behaviour might be manipulated therapeutically.

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