scholarly journals Barley stripe mosaic virus infection requires PKA-mediated phosphorylation of γb for suppression of both RNA silencing and the host cell death response

2018 ◽  
Vol 218 (4) ◽  
pp. 1570-1585 ◽  
Author(s):  
Xuan Zhang ◽  
Kai Dong ◽  
Kai Xu ◽  
Kun Zhang ◽  
Xuejiao Jin ◽  
...  
2020 ◽  
Vol 245 ◽  
pp. 153110 ◽  
Author(s):  
Pedro Filho Noronha Souza ◽  
Jose Tadeu Abreu Oliveira ◽  
Ilka Maria Vasconcelos ◽  
Vladimir Gonçalves Magalhães ◽  
Fredy Davi Albuquerque Silva ◽  
...  

2001 ◽  
Vol 14 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Anthony B. Cole ◽  
Lóránt Király ◽  
Kathleen Ross ◽  
James E. Schoelz

Cauliflower mosaic virus strain W260 elicits a hypersensitive response (HR) in leaves of Nicotiana edwardsonii, an interspecific hybrid derived from a cross between N. glutinosa and N. clevelandii. Interestingly, we found that N. glutinosa is resistant to W260, but responds with local chlorotic lesions rather than necrotic lesions. In contrast, N. clevelandii responds to W260 with systemic cell death. The reactions of the progenitors of N. edwardsonii to W260 infection indicated that each contributed a factor toward the development of HR. In this study, we present two lines of evidence to show that the resistance and cell death that comprise the HR elicited by W260 can indeed be uncoupled. First, we showed that the non-necrotic resistance response of N. glutinosa could be converted to HR when these plants were crossed with N. clevelandii. Second, we found that cell death and resistance segregated independently in the F2 population of a cross between N. edwardsonii and N. clevelandii. We concluded that the resistance of N. edwardsonii to W260 infection was conditioned by a gene derived from N. glutinosa, whereas cell death was conditioned by a gene derived from N. clevelandii. An analysis of pathogenesis-related (PR) protein expression in response to W260 infection revealed that elicitation of PR proteins was associated with resistance rather than with the onset of cell death.


2017 ◽  
Vol 5 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Guoxin Wang ◽  
Ling Wang ◽  
Yu Cui ◽  
Meihua Yu ◽  
Chen Dang ◽  
...  

2004 ◽  
Vol 5 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Tom Van Den Boogaart ◽  
Andrew J. Maule ◽  
Jeffrey W. Davies ◽  
George P. Lomonossoff

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ayushi Chaurasiya ◽  
Swati Garg ◽  
Ashish Khanna ◽  
Chintam Narayana ◽  
Ved Prakash Dwivedi ◽  
...  

AbstractHijacking of host metabolic status by a pathogen for its regulated dissemination from the host is prerequisite for the propagation of infection. M. tuberculosis secretes an NAD+-glycohydrolase, TNT, to induce host necroptosis by hydrolyzing Nicotinamide adenine dinucleotide (NAD+). Herein, we expressed TNT in macrophages and erythrocytes; the host cells for M. tuberculosis and the malaria parasite respectively, and found that it reduced the NAD+ levels and thereby induced necroptosis and eryptosis resulting in premature dissemination of pathogen. Targeting TNT in M. tuberculosis or induced eryptosis in malaria parasite interferes with pathogen dissemination and reduction in the propagation of infection. Building upon our discovery that inhibition of pathogen-mediated host NAD+ modulation is a way forward for regulation of infection, we synthesized and screened some novel compounds that showed inhibition of NAD+-glycohydrolase activity and pathogen infection in the nanomolar range. Overall this study highlights the fundamental importance of pathogen-mediated modulation of host NAD+ homeostasis for its infection propagation and novel inhibitors as leads for host-targeted therapeutics.


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