Trafficking modulator TENin1 inhibits endocytosis, causes endomembrane protein accumulation at the pre-vacuolar compartment and impairs gravitropic response in Arabidopsis thaliana

2014 ◽  
Vol 464 (2) ◽  
pp. 291-291
Author(s):  
R. Paudyal ◽  
A. Jamaluddin ◽  
J. P. Warren ◽  
S. M. Doyle ◽  
S. Robert ◽  
...  
2014 ◽  
Vol 460 (2) ◽  
pp. 177-185 ◽  
Author(s):  
Rupesh Paudyal ◽  
Adam Jamaluddin ◽  
James P. Warren ◽  
Siamsa M. Doyle ◽  
Stéphanie Robert ◽  
...  

In the present study a detailed characterization of a small molecule inhibitor of protein trafficking and gravitropic response is described. We also identified two Arabidopsis thaliana ecotypes that display resistance to this compound. The ecotypes and chemical provide useful tool to investigate protein trafficking.


2011 ◽  
Vol 67 (5) ◽  
pp. 817-826 ◽  
Author(s):  
Hana Rakusová ◽  
Javier Gallego-Bartolomé ◽  
Marleen Vanstraelen ◽  
Hélène S. Robert ◽  
David Alabadí ◽  
...  

2010 ◽  
Vol 21 (7) ◽  
pp. 1263-1271 ◽  
Author(s):  
Naxhiely Martínez Ramón ◽  
Bonnie Bartel

Peroxisomes compartmentalize certain metabolic reactions critical to plant and animal development. The import of proteins from the cytosol into the organelle matrix depends on more than a dozen peroxin (PEX) proteins, with PEX5 and PEX7 serving as receptors that shuttle proteins bearing one of two peroxisome-targeting signals (PTSs) into the organelle. PEX5 is the PTS1 receptor; PEX7 is the PTS2 receptor. In plants and mammals, PEX7 depends on PEX5 binding to deliver PTS2 cargo into the peroxisome. In this study, we characterized a pex7 missense mutation, pex7-2, that disrupts both PEX7 cargo binding and PEX7-PEX5 interactions in yeast, as well as PEX7 protein accumulation in plants. We examined localization of peroxisomally targeted green fluorescent protein derivatives in light-grown pex7 mutants and observed not only the expected defects in PTS2 protein import but also defects in PTS1 import. These PTS1 import defects were accompanied by reduced PEX5 accumulation in light-grown pex7 seedlings. Our data suggest that PEX5 and PTS1 import depend on the PTS2 receptor PEX7 in Arabidopsis and that the environment may influence this dependence. These data advance our understanding of the biogenesis of these essential organelles and provide a possible rationale for the retention of the PTS2 pathway in some organisms.


1996 ◽  
Vol 110 (3) ◽  
pp. 933-943 ◽  
Author(s):  
H. Fukaki ◽  
H. Fujisawa ◽  
M. Tasaka

2015 ◽  
Vol 62 (5) ◽  
pp. 664-669 ◽  
Author(s):  
Z. Q. Yan ◽  
H. Jin ◽  
D. D. Wang ◽  
X. Y. Yang ◽  
B. Qin

2018 ◽  
Vol 85 (2) ◽  
pp. 211-220 ◽  
Author(s):  
Zhiqiang Yan ◽  
Dandan Wang ◽  
Haiyan Cui ◽  
Yuhe Sun ◽  
Xiaoyan Yang ◽  
...  

2017 ◽  
Vol 114 (24) ◽  
pp. E4884-E4893 ◽  
Author(s):  
Elke Barbez ◽  
Kai Dünser ◽  
Angelika Gaidora ◽  
Thomas Lendl ◽  
Wolfgang Busch

Plant cells are embedded within cell walls, which provide structural integrity, but also spatially constrain cells, and must therefore be modified to allow cellular expansion. The long-standing acid growth theory postulates that auxin triggers apoplast acidification, thereby activating cell wall-loosening enzymes that enable cell expansion in shoots. Interestingly, this model remains heavily debated in roots, because of both the complex role of auxin in plant development as well as technical limitations in investigating apoplastic pH at cellular resolution. Here, we introduce 8-hydroxypyrene-1,3,6-trisulfonic acid trisodium salt (HPTS) as a suitable fluorescent pH indicator for assessing apoplastic pH, and thus acid growth, at a cellular resolution in Arabidopsis thaliana roots. Using HPTS, we demonstrate that cell wall acidification triggers cellular expansion, which is correlated with a preceding increase of auxin signaling. Reduction in auxin levels, perception, or signaling abolishes both the extracellular acidification and cellular expansion. These findings jointly suggest that endogenous auxin controls apoplastic acidification and the onset of cellular elongation in roots. In contrast, an endogenous or exogenous increase in auxin levels induces a transient alkalinization of the extracellular matrix, reducing cellular elongation. The receptor-like kinase FERONIA is required for this physiological process, which affects cellular root expansion during the gravitropic response. These findings pinpoint a complex, presumably concentration-dependent role for auxin in apoplastic pH regulation, steering the rate of root cell expansion and gravitropic response.


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