Osmotic Stress Modulates the Balance between Exocytosis and Clathrin-Mediated Endocytosis in Arabidopsis thaliana

Abstract

The sessile life style of plants creates the need to deal with an often adverse environment, in which water availability can change on a daily basis, challenging the cellular physiology and integrity. Changes in osmotic conditions disrupt the equilibrium of the plasma membrane: hypoosmotic conditions increase and hyperosmotic environment decrease the cell volume. Here, we show that short-term extracellular osmotic treatments are closely followed by a shift in the balance between endocytosis and exocytosis in root meristem cells. Acute hyperosmotic treatments (ionic and nonionic) enhance clathrin-mediated endocytosis simultaneously attenuating exocytosis, whereas hypoosmotic treatments have the opposite effects. In addition to clathrin recruitment to the plasma membrane, components of early endocytic trafficking are essential during hyperosmotic stress responses. Consequently, growth of seedlings defective in elements of clathrin or early endocytic machinery is more sensitive to hyperosmotic treatments. We also found that the endocytotic response to a change of osmotic status in the environment is dominant over the presumably evolutionary more recent regulatory effect of plant hormones, such as auxin. These results imply that osmotic perturbation influences the balance between endocytosis and exocytosis acting through clathrin-mediated endocytosis. We propose that tension on the plasma membrane determines the addition or removal of membranes at the cell surface, thus preserving cell integrity.

Halotropism requires phospholipase Dζ1‐mediated modulation of cellular polarity of auxin transport carriers

“…This is in agreement with previously shown involvement of PLDζ2 in auxin carrier relocalization during halotropism (Galvan‐Ampudia et al, ). Also, we found similar initial sorbitol‐induced internalization of PIN2 compared with previously reported PIN2 dynamics after a 10‐min mannitol treatment (Zwiewka, Nodzynski, Robert, Vanneste, & Friml, ). However, although salt induces a relocalization of PIN2 to the lateral membrane compartment, osmotic stress does not have this effect.…”

CELLULOSE SYNTHASE INTERACTIVE1 Is Required for Fast Recycling of Cellulose Synthase Complexes to the Plasma Membrane in Arabidopsis

“…Although detailed molecular mechanisms linking abiotic stress and endocytosis in plants are lacking, saline or osmotic stress does trigger the activation of endocytic uptake of a biotinylated endocytic marker in rice cells (Bahaji et al, 2003), and overexpression of At-Rab7 increases salt and osmotic stress tolerance, which is consistent with accelerated membrane endocytosis (Mazel et al, 2004). Furthermore, genetic studies have demonstrated the importance of endocytosis for plant fitness under stress (Leshem et al, 2007;Bar et al, 2008aBar et al, , 2008bZwiewka et al, 2015). These observations have led to the hypothesis that plants have developed a more efficient internalization mechanism to retrieve membrane materials to help them adapt to abiotic stress.…”

Vesicular trafficking and salinity responses in plants

“…Intriguingly, salinity induces a dramatic relocalization of GFP‐tagged ARA6QL protein to the PM, suggesting a function of the protein at the PM under salt stress . A recent study also reports an increase in the size of ARA6‐positive compartments under salt stress , although the implications of this observation have not been followed up. Plants with a functionally compromised VPS9a protein, the Guanine nucleotide exchange factor for the Rab5 homologs, are extremely salt‐sensitive .…”

“…The contribution of CME and CIE pathways to the salt‐induced escalation of endocytosis is an area of active research. Reports of enhanced endocytosis through the clathrin‐mediated pathway are based on the observed rise in clathrin recruitment to the PM , whereas others report that clathrin‐independent pathways are also boosted . Salt‐induced increase in FM4‐64 uptake is observed even in the presence of genetic and chemical perturbation of clathrin although the extent of enhancement is substantially reduced.…”