The Great Irish Potato Famine

2000 ◽  
Vol 26/27 ◽  
pp. 131 ◽  
Author(s):  
Ronald Rudin ◽  
James S. Donnelly,
2014 ◽  
Vol 70 (a1) ◽  
pp. C826-C826
Author(s):  
Abbas Maqbool ◽  
Richard Richard ◽  
Tolga Bozkurt ◽  
Yasin Dagdas ◽  
Khaoula Belhai ◽  
...  

Autophagy is a catabolic process involving degradation of dysfunctional cytoplasmic components to ensure cellular survival under starvation conditions. The process involves formation of double-membrane vesicles called autophagosomes and delivery of the inner constituents to lytic compartments. It can also target invading pathogens, such as intracellular bacteria, for destruction and is thus implicated in innate immune pathways [1]. In response, certain mammalian pathogens deliver effector proteins into host cells that inhibit autophagy and contribute to enabling parasitic infection [2]. Pyhtophthora infestans, the Irish potato famine pathogen, is a causative agent of late blight disease in potato and tomato crops. It delivers a plethora of modular effector proteins into plant cells to promote infection. Once inside the cell, RXLR-type effector proteins engage with host cell proteins, to manipulate host cell physiology for the benefit of the pathogen. As plants lack an adaptive immune system, this provides a robust mechanism for pathogens to circumvent host defense. PexRD54 is an intracellular RXLR-type effector protein produced by P. infestans. PexRD54 interacts with potato homologues of autophagy protein ATG8 in plant cells. We have been investigating the structural and biochemical basis of the PexRD54/ATG8 interaction in vitro. We have purified PexRD54 and ATG8 independently and in complex from E. coli. Using protein/protein interaction studies we have shown that PexRD54 binds ATG8 with sub-micromolar affinity. We have also determined the structure of PexRD54 in the presence of ATG8. This crystal structure provides key insights into how the previously reported WY-fold of oomycete RXLR-type effectors [3] can be organized in multiple repeats. The structural data also provides insights into the interaction between PexRD54 and ATG8, suggesting further experiments to understand the impact of this interaction on host cell physiology and how this benefits the pathogen.


BioScience ◽  
1997 ◽  
Vol 47 (6) ◽  
pp. 363-371 ◽  
Author(s):  
William E. Fry ◽  
Stephen B. Goodwin

2021 ◽  
Author(s):  
Erin K. Zess ◽  
Yasin F. Dagdas ◽  
Esme Peers ◽  
Abbas Maqbool ◽  
Mark J. Banfield ◽  
...  

AbstractIn order to infect a new host species, the pathogen must evolve to enhance infection and transmission in the novel environment. Although we often think of evolution as a process of accumulation, it is also a process of loss. Here, we document an example of regressive evolution in the Irish potato famine pathogen (Phytophthora infestans) lineage, providing evidence that a key sequence motif in the effector PexRD54 has degenerated following a host jump. We began by looking at PexRD54 and PexRD54-like sequences from across Phytophthora species. We found that PexRD54 emerged in the common ancestor of Phytophthora clade 1b and 1c species, and further sequence analysis showed that a key functional motif, the C-terminal ATG8-interacting motif (AIM), was also acquired at this point in the lineage. A closer analysis showed that the P. mirabilis PexRD54 (PmPexRD54) AIM appeared unusual, the otherwise-conserved central residue mutated from a glutamate to a lysine. We aimed to determine whether this PmPexRD54 AIM polymorphism represented an adaptation to the Mirabilis jalapa host environment. We began by characterizing the M. jalapa ATG8 family, finding that they have a unique evolutionary history compared to previously characterized ATG8s. Then, using co-immunoprecipitation and isothermal titration calorimetry assays, we showed that both full-length PmPexRD54 and the PmPexRD54 AIM peptide bind very weakly to the M. jalapa ATG8s. Through a combination of binding assays and structural modelling, we showed that the identity of the residue at the position of the PmPexRD54 AIM polymorphism can underpin high-affinity binding to plant ATG8s. Finally, we conclude that the functionality of the PexRD54 AIM was lost in the P. mirabilis lineage, perhaps owing to as-yet-unknown pressure on this effector in the new host environment.Author SummaryPathogens evolve in concert with their hosts. When a pathogen begins to infect a new host species, known as a “host jump,” the pathogen must evolve to enhance infection and transmission. These evolutionary processes can involve both the gain and loss of genes, as well as dynamic changes in protein function. Here, we describe an example of a pathogen protein that lost a key functional domain following a host jump, a salient example of “regressive evolution.” Specifically, we show that an effector protein from the plant pathogen Phytopthora mirabilis, a host-specific lineage closely related to the Irish potato famine pathogen Phytopthora infestans, has a derived amino acid polymorphism that results in a loss of interaction with certain host machinery.


2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Marina Pais ◽  
Kentaro Yoshida ◽  
Artemis Giannakopoulou ◽  
Mathieu A. Pel ◽  
Liliana M. Cano ◽  
...  

2014 ◽  
Vol 91 (6) ◽  
pp. 579-593 ◽  
Author(s):  
Yeen Ting Hwang ◽  
Champa Wijekoon ◽  
Melanie Kalischuk ◽  
Dan Johnson ◽  
Ron Howard ◽  
...  

Author(s):  
Barry Riley

Even while attempting to avoid “entangling alliances,” the elected officials of the newly formed United States were, as early as 1794, debating whether the government should provide economic aid to destitute residents of a foreign country. Congressman James Madison argued that the Constitution contained no authority allowing it. Others argued that it was not the intention of the founding fathers to prevent such acts of benevolence. For 120 years these arguments would be resurrected whenever a major calamity threatened innocent foreign residents with hunger and famine. Only occasionally would assistance be provided. Much more often, as with the Irish potato famine of the 1840s, there would be no provision of food aid to prevent starvation.


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