scholarly journals Involvement of N-acylhomoserine Lactones Throughout Plant Infection by Erwinia carotovora subsp. atroseptica (Pectobacterium atrosepticum)

2004 ◽  
Vol 17 (11) ◽  
pp. 1269-1278 ◽  
Author(s):  
Bruno Smadja ◽  
Xavier Latour ◽  
Denis Faure ◽  
Sylvie Chevalier ◽  
Yves Dessaux ◽  
...  

Erwinia carotovora subsp. atroseptica is responsible for potato blackleg disease in the field and tuber soft rot during crop storage. The process leading to the disease occurs in two phases: a primary invasion step followed by a maceration step. Bacteria-to-bacteria communication is associated with a quorum-sensing (QS) process based on the production of N-acylhomoserine lactones (HSL). The role of HSL throughout plant infection was analyzed. To this purpose, HSL produced by a specific E. carotovora subsp. atroseptica wild-type strain, which was particularly virulent on potato, were identified. A derivative of this strain that expressed an HSL lactonase gene and produced low amounts of HSL was generated. The comparison of these strains allowed the evaluation of the role of HSL and QS in disease establishment and development. Bacterial growth and motility; activity of proteins secreted by type I, II, and III systems; and hypersensitive and maceration reactions were evaluated. Results indicated that HSL production and QS regulate only those traits involved in the second stage of the host plant infection (i.e., tissue maceration) and hypersensitive response in nonhost tobacco plants. Therefore, the use of QS quenching strategies for biological control in E. carotovora subsp. atroseptica cannot prevent initial infection and multiplication of this pathogen.

HortScience ◽  
1997 ◽  
Vol 32 (3) ◽  
pp. 512A-512 ◽  
Author(s):  
M.V. Bhaskara Reddy ◽  
Alain Asselin ◽  
Joseph Arul

We have investigated the relationship between chitosan treatments and maceration of potato tissue by macerating enzymes secreted by Erwinia carotovora causal agent of soft rot of potato. Erwinia isolated from potato showing soft rot symptoms was used for inoculation. The bacteria secreted a wide spectrum of enzymes that degraded potato cell walls. Polygalacturonase (PG), pectate lyase (PL), pectinmethylesterase (PME), cellulase, xylanase, and protease showed the highest activity in potato tissue inoculated with the pathogen. Accordingly increased maceration and cell death were observed. On the other hand, in chitosan-treated tissue and challenged with the pathogen, significant decrease in enzymatic activity and tissue maceration were observed, more so with increasing chitosan concentration. This observation confirmed that chitosan interfered with multiplication and pathogenic powers of the bacteria, thereby improving cell texture and viability. Crude extracts obtained from treatments were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to assess pectinase activity. The electophoretic profiles showed significant lytic zone of pectin degradation in the control, which decreased with increase in chitosan concentrations. No lytic zone was observed at 8 mg·ml–1 chitosan concentration and was comparable to intact activity in untreated potato tissue. Pectic enzyme reaction products were analyzed to see the action pattern of pectinases in the crude extracts. Cellulose choromatographic profiles revealed monomers and dimers of polygalacturonic acid up to 6 mg·ml–1 chitosan concentrations. The results suggest that chitosan significantly inhibits bacterial growth and the production of macerating enzymes by the pathogen and thus chitosan can be a potential anti-bacterial agent.


1998 ◽  
Vol 66 (3) ◽  
pp. 1159-1166 ◽  
Author(s):  
Masayuki Tokuda ◽  
Thonthi Karunakaran ◽  
Margaret Duncan ◽  
Nobushiro Hamada ◽  
Howard Kuramitsu

ABSTRACT In order to access the role of the Porphyromonas gingivalis Arg-gingipain proteases in the virulence of this organism, a mutant defective in the rgpA gene was constructed in strain 381. This mutant, MT10, displayed only 40% of the Arg-specific cysteine protease activity of the wild-type strain. In addition, MT10, as well as the recently characterized protease mutant G-102, which is defective in the rgpB gene, displayed reduced self-aggregation, hemagglutination, and the ability to bind to immobilized type I collagen compared to levels of the wild-type parent. However, unlike mutant G-102, the rgpA mutant displayed increased binding to epithelial cells relative to that of the parental organism. Mutant MT10 also did not express detectable levels of the FimA protein as assessed by both Western and Northern blotting or fimbriae visible by electron microscopy of the cells. Furthermore, the ability of MT10 to degrade rat tail collagen fibers when it was cultured at 37°C was markedly attenuated compared to that of strain 381. These results suggest that Arg-gingipain A may play a significant role in the pathogenicity of P. gingivalis by altering the colonization and toxic properties of the organism.


1998 ◽  
Vol 64 (6) ◽  
pp. 546-551
Author(s):  
S.M. Khorshed ALAM ◽  
Jiro TOGASHI ◽  
Tsuneo NAMAI ◽  
Koushi UEDA

2014 ◽  
Vol 60 (5) ◽  
pp. 297-305 ◽  
Author(s):  
Yuta Ogata ◽  
Hiroki Katoh ◽  
Munehiko Asayama ◽  
Shigeru Chohnan

Pantothenate kinases (CoaAs) catalyze the phosphorylation of pantothenate in the first step of the coenzyme A (CoA) biosynthetic pathway. These bacterial enzymes have been categorized into 3 types, the prokaryotic type I, II, and III CoaAs. Bacteria typically carry a single CoaA gene on their genome, but Bacillus subtilis possesses 2 proteins homologous to type I and III CoaAs, known as BsCoaA and BsCoaX, respectively. Both recombinant proteins exhibited the expected kinase activity and the characteristic properties of type I and III CoaAs, i.e., regulation by CoASH and acyl-CoAs in BsCoaA and the requirement of a monovalent cation in BsCoaX. Both gene disruptants appeared to grow in a manner similar to the wild-type strain. With the BsCoaX disruptant, the BsCoaA had the ability to completely fill the intracellular CoA pool, whereas the BsCoaA disruptant did not. These findings clearly indicate that these 2 CoaAs are employed together in the CoA biosynthetic pathway in B. subtilis and that the contribution of the type I CoaA (BsCoaA) to the formation of the intracellular CoA pool is larger than that of the type III CoaA (BsCoaX).


2020 ◽  
Vol 20 (12) ◽  
pp. 1074-1092 ◽  
Author(s):  
Rammohan R.Y. Bheemanaboina

Phosphoinositide 3-kinases (PI3Ks) are a family of ubiquitously distributed lipid kinases that control a wide variety of intracellular signaling pathways. Over the years, PI3K has emerged as an attractive target for the development of novel pharmaceuticals to treat cancer and various other diseases. In the last five years, four of the PI3K inhibitors viz. Idelalisib, Copanlisib, Duvelisib, and Alpelisib were approved by the FDA for the treatment of different types of cancer and several other PI3K inhibitors are currently under active clinical development. So far clinical candidates are non-selective kinase inhibitors with various off-target liabilities due to cross-reactivities. Hence, there is a need for the discovery of isoform-selective inhibitors with improved efficacy and fewer side-effects. The development of isoform-selective inhibitors is essential to reveal the unique functions of each isoform and its corresponding therapeutic potential. Although the clinical effect and relative benefit of pan and isoformselective inhibition will ultimately be determined, with the development of drug resistance and the demand for next-generation inhibitors, it will continue to be of great significance to understand the potential mechanism of isoform-selectivity. Because of the important role of type I PI3K family members in various pathophysiological processes, isoform-selective PI3K inhibitors may ultimately have considerable efficacy in a wide range of human diseases. This review summarizes the progress of isoformselective PI3K inhibitors in preclinical and early clinical studies for anticancer and other various diseases.


2009 ◽  
Vol 5 (2) ◽  
pp. 143-149
Author(s):  
Marja Ojaniemi ◽  
Mari Liljeroos ◽  
Reetta Vuolteenaho

2020 ◽  
Vol 16 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Ashraf Okba ◽  
Salwa Seddik Hosny ◽  
Alyaa Elsherbeny ◽  
Manal Mohsin Kamal

Background and Aims: Women who develop GDM (gestational diabetes mellitus) have a relative insulin secretion deficiency, the severity of which may be predictive for later development of diabetes. This study aimed to investigate the role of fasting plasma glucagon in the prediction of later development of diabetes in pregnant women with GDM. Materials and Methods: The study was conducted on 150 pregnant women with GDM after giving informed oral and written consents and being approved by the research ethical committee according to the declaration of Helsinki. The study was conducted in two phases, first phase during pregnancy and the second one was 6 months post-partum, as we measured fasting plasma glucagon before and after delivery together with fasting and 2 hour post-prandial plasma sugar. Results: Our findings suggested that glucagon levels significantly increased after delivery in the majority 14/25 (56%) of GDM women who developed type 2 DM within 6 months after delivery compared to 6/20 (30%) patients with impaired fasting plasma glucose (IFG) and only 22/105 (20%) non DM women, as the median glucagon levels were 80,76, 55, respectively. Also, there was a high statistical difference between fasting plasma glucagon post-delivery among diabetic and non-diabetic women (p ≤ 0.001). These results indicated the useful role of assessing fasting plasma glucagon before and after delivery in patients with GDM to predict the possibility of type 2 DM. Conclusion: There is a relatively high glucagon level in GDM patients, which is a significant pathogenic factor in the incidence of subsequent diabetes in women with a history of GDM. This could be important in the design of follow-up programs for women with previous GDM.


Sign in / Sign up

Export Citation Format

Share Document