scholarly journals Barley RIC157 is involved in RACB-mediated susceptibility to powdery mildew

2019 ◽  
Author(s):  
Stefan Engelhardt ◽  
Michaela Kopischke ◽  
Johanna Hofer ◽  
Katja Probst ◽  
Christopher McCollum ◽  
...  

AbstractSuccessful pathogens often benefit from certain cellular host processes. For the biotrophic ascomycete fungus Blumeria graminis f.sp. hordei (Bgh) it has been shown that barley RACB, a small monomeric G-protein (ROP, RHO of plants), is required for full susceptibility to fungal penetration. The susceptibility function of RACB probably lies in its role in cell polarisation, which may be co-opted by the pathogen for invasive ingrowth of its haustorium. However, the actual mechnism of how RACB supports the fungal penetration success is little understood. RIC proteins are considered scaffold proteins which can interact directly with ROPs via a conserved CRIB motif. Here we describe a yet uncharacterised RIC protein, RIC157, which can interact directly with RACB. We could show that RIC157 undergoes a recruitment from the cytoplasm to the cell periphery in the presence of activated RACB. During fungal infection, RIC157 and activated RACB colocalise at the penetration site, particularly at the haustorial neck. In a RACB-dependent manner, transiently overexpressed RIC157 renders barley epidermal cells more susceptible to fungal penetration. We conclude that RIC157 promotes fungal penetration into barley epidermal cells via its function as downstream executor in RACB-signaling.

2000 ◽  
Vol 78 (12) ◽  
pp. 1561-1570 ◽  
Author(s):  
D Rubiales ◽  
T LW Carver

The histology of resistance to infection by Blumeria graminis DC Speer f.sp. hordei, Blumeria graminis f.sp. tritici, and Blumeria graminis f.sp. avenae was studied in 15 accession lines of Hordeum chilense. All were highly resistant to all formae speciales. There were small differences in spore germination rates and the morphological normality of germlings formed on the different lines. Relatively large differences between accessions were detected in terms of penetration resistance and the frequency with which attacked epidermal cells died. Greater penetration resistance was expressed by epidermal cells of the seventh-formed leaves than by earlier leaves, indicating that penetration resistance is a component of adult plant resistance in H. chilense. Epidermal cells overlying vascular tissues (long epidermal cells) were more resistant to penetration than cells adjacent or close to stomatal complexes. In a limited examination involving two accession lines, epidermal cells on the abaxial leaf surface of one line were more penetration resistant than those on the adaxial surface; the other line was highly resistant on both surfaces. However, in the few cases where long cells and abaxial cells were penetrated, the frequency of associated cell death was lower than in short cells or on the adaxial leaf surface. This is consistent with the macroscopic observation that the few colonies formed on H. chilense were often close to the mid-rib and more frequent on the abaxial leaf surface. The data support the view that H. chilense offers a valuable source of powdery mildew resistance for cultivated cereals.Key words: Blumeria graminis, Erysiphe graminis, powdery mildew, disease resistance, histology, Hordeum chilense.


Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 879-892 ◽  
Author(s):  
Anatoly V Grishin ◽  
Michael Rothenberg ◽  
Maureen A Downs ◽  
Kendall J Blumer

Abstract In the yeast Saccharomyces cerevisiae, mating pheromone response is initiated by activation of a G protein- and mitogen-activated protein (MAP) kinase-dependent signaling pathway and attenuated by several mechanisms that promote adaptation or desensitization. To identify genes whose products negatively regulate pheromone signaling, we screened for mutations that suppress the hyperadaptive phenotype of wild-type cells overexpressing signaling-defective G protein β subunits. This identified recessive mutations in MOT3, which encodes a nuclear protein with two Cys2-His2 Zn fingers. MOT3 was found to be a dosage-dependent inhibitor of pheromone response and pheromone-induced gene expression and to require an intact signaling pathway to exert its effects. Several results suggested that Mot3 attenuates expression of pheromone-responsive genes by mechanisms distinct from those used by the negative transcriptional regulators Cdc36, Cdc39, and Mot2. First, a Mot3-lexA fusion functions as a transcriptional activator. Second, Mot3 is a dose-dependent activator of several genes unrelated to pheromone response, including CYC1, SUC2, and LEU2. Third, insertion of consensus Mot3 binding sites (C/A/T)AGG(T/C)A activates a promoter in a MOT3-dependent manner. These findings, and the fact that consensus binding sites are found in the 5′ flanking regions of many yeast genes, suggest that Mot3 is a globally acting transcriptional regulator. We hypothesize that Mot3 regulates expression of factors that attenuate signaling by the pheromone response pathway.


2011 ◽  
Vol 47 (No. 3) ◽  
pp. 95-100 ◽  
Author(s):  
A. Dreiseitl

  The resistance Heils Hanna (HH) was postulated in several tens of 471 previously tested winter barley cultivars. In this paper, new tests on 29 of these cultivars are reported. Thirty-two reference isolates of Blumeria graminis f.sp. hordei held in the pathogen genebank at the Agricultural Research Institute in Kromeriz, Ltd. including a Japanese isolate and five Israeli isolates were used for response tests. However, the resistance HH conferred by the gene Mla8 and herein characterised by reaction type 0 to an old Japanese isolate known as Race I was now postulated only in four cultivars. In the other 25 cultivars another resistance, characterised by reaction type 0 to Race I and also to two Israeli isolates, was detected. In addition to the two mentioned resistances, eight known (Bw, Dr2, Ha, IM9, Ln, Lv, Ra and Sp) resistances were found in the set examined. Lomerit was the only registered cultivar tested here in which the newly detected resistance was present alone, therefore, it is recommended that this resistance be designated Lo.


1990 ◽  
Vol 10 (6) ◽  
pp. 3277-3279 ◽  
Author(s):  
G Tjaden ◽  
A Aguanno ◽  
R Kumar ◽  
D Benincasa ◽  
R M Gubits ◽  
...  

Nerve growth factor (NGF) affects levels of the alpha subunit of the stimulatory G protein (Gs-alpha) in pheochromocytoma 12 cells in a bidirectional, density-dependent manner. Cells grown at high density responded to NGF treatment with increased levels of Gs-alpha mRNA and protein. Conversely, in cells grown in low-density cultures, levels of this mRNA were lowered by NGF treatment.


2000 ◽  
Vol 78 (10) ◽  
pp. 1288-1293 ◽  
Author(s):  
Jérôme Muchembled ◽  
Anissa Lounès-Hadj Sahraoui ◽  
Anne Grandmougin-Ferjani ◽  
Michel Sancholle

The total sterol composition of conidia of the obligate plant pathogen Blumeria (= Erysiphe) graminis f.sp. tritici has been analysed as a function of their ontogeny during sporulation. Two main classes of sterols were characterized: 24-ethylsterols (24-ethylcholesta-5,22-dienol, 24-ethylcholesterol, and Δ5-avenasterol) and 24-methylsterols (24-methylenecholesterol and episterol). Our results show that sterol composition is greatly modified during ontogeny of B. graminis conidia both at the qualitative and quantitative levels. In particular, 24-methylsterols, e.g., 24-methylenecholesterol and episterol, are the major sterols in old conidia whereas 24-ethylsterols, e.g., 24-ethylcholesta-5,22-dienol, 24-ethylcholesterol, and Δ5-avenasterol, are the main sterols in young conidia.Key words: Erysiphe, wheat powdery mildew, sterols, ontogeny.


1975 ◽  
Vol 53 (22) ◽  
pp. 2589-2597 ◽  
Author(s):  
H. H. Edwards

M1-a-mediated resistance in barley to invasion by the CR3 race of Erysiphe graminis f. sp. hordei does not occur in every host cell with the same speed and severity. In some cells ultrastructural changes within the host cell as a result of resistance will occur within 24 h after inoculation, whereas in other cells these changes may take up to 72 h. In some cells the ultrastructural changes are so drastic that they give the appearance of a hypersensitive death of the host cell, whereas in other cells the changes are very slight. In any case, at the end of these changes the fungus ceases growth. The ultrastructural changes occur in penetrated host epidermal cells as well as non-infected adjacent epidermal and mesophyll cells.The following ultrastructural changes have been observed: (1) an electron-dense material which occurs either free in the vacuole or adhering to the tonoplast (the material is granular or in large clumps); (2) an increased electron density of the host cytoplasm and nucleus; (3) a breakdown of the tonoplast so that the cytoplasmic constituents become dispersed throughout the cell lumen; and (4) the deposition of papillar-like material in areas other than the penetration site. The first three changes take place within the host cell protoplasts and are directly attributable to the gene M1-a. These changes are typical of stress or incompatibility responses and thus M1-a appears to trigger a generalized incompatibility response in the presence of race CR3. The papillar-like material occurs outside the host cell protoplast in the same manner as the papilla and probably is not directly attributable to M1-a.


1994 ◽  
Vol 304 (2) ◽  
pp. 531-536 ◽  
Author(s):  
H Ohnishi ◽  
T Mine ◽  
I Kojima

It has recently been shown that somatostatin inhibits amylase secretion from isolated pancreatic acini by reducing cyclic AMP (cAMP) production [Matsushita, Okabayashi, Hasegawa, Koide, Kido, Okutani, Sugimoto and Kasuga (1993) Gastroenterology 104, 1146-1152]. To date, however, little is known as to the other mechanism(s) by which somatostatin inhibits amylase secretion in exocrine pancreas. To investigate the action of somatostatin independent of cAMP generation, we examined the effect of somatostatin in isolated rat pancreatic acini stimulated by 1 microM calcium ionophore A23187 and 1 mM 8-bromo-cyclic AMP (8Br-cAMP). Somatostatin inhibited amylase secretion evoked by a combination of A23187 and 8Br-cAMP in a dose-dependent manner. The maximum inhibition was obtained by 10(-7) M somatostatin, and at this concentration somatostatin inhibited the effect of A23187 and 8Br-cAMP by approximately 30%. In electrically permeabilized acini, an elevation of free calcium concentration resulted in an increase in amylase secretion and cAMP enhanced the secretion evoked by calcium. cAMP shifted the dose-response curve for calcium-induced secretion leftwards and elevated the peak value of secretion. Somatostatin inhibited the effect of cAMP on calcium-induced amylase secretion by shifting the dose-response curve to the right. To determine the involvement of a G-protein(s), we examined the effect of somatostatin in acini pretreated with pertussis toxin. Pretreatment of acini with pertussis toxin completely blocked somatostatin-inhibition of amylase-secretion evoked by A23187 and 8Br-cAMP. These results indicate that somatostatin decreases amylase secretion induced by cAMP and calcium by reducing the calcium sensitivity of exocytosis. A pertussis toxin-sensitive G-protein is also involved in this step.


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