scholarly journals Hijacking of the host cell Golgi by Plasmodium berghei liver stage parasites

2021 ◽  
Author(s):  
Mariana De Niz ◽  
Reto Caldelari ◽  
Gesine Kaiser ◽  
Benoit Zuber ◽  
Won Do Heo ◽  
...  

The intracellular lifestyle represents a challenge for the rapidly proliferating liver stage Plasmodium parasite. In order to scavenge host resources, Plasmodium has evolved the ability to target and manipulate host cell organelles. Using dynamic fluorescence-based imaging, we show an interplay between the pre-erythrocytic stages of Plasmodium berghei and the host cell Golgi during liver stage development. Liver stage schizonts fragment the host cell Golgi into miniaturized stacks, which increases surface interactions with the parasite's parasitophorous vacuolar membrane. Expression of specific dominant-negative Arf1 and Rab GTPases to interfere with the host cell Golgi-linked vesicular machinery resulted in developmental delay and diminished survival of liver stage parasites. Moreover, functional Rab11a is critical for the parasites ability to induce Golgi fragmentation. Altogether, we demonstrate that the structural integrity of the host cell Golgi and Golgi-associated vesicular traffic is important for optimal pre-erythrocytic development of P. berghei. The parasite hijacks the hepatocyte's Golgi structure to optimize its own intracellular development.

2020 ◽  
Author(s):  
Mariana De Niz ◽  
Gesine Kaiser ◽  
Benoit Zuber ◽  
Won Do Heo ◽  
Volker T. Heussler ◽  
...  

AbstractThe intracellular lifestyle represents a challenge for the rapidly proliferating liver stage Plasmodium parasite. In order to scavenge host resources, Plasmodium has evolved the ability to target and manipulate host cell organelles. Using dynamic fluorescence-based imaging, we show a direct interplay between the pre-erythrocytic stages of Plasmodium berghei and the host cell Golgi during the entire liver stage development. Liver stage schizonts fragment the host cell Golgi into miniaturized stacks, which increases surface interactions with the parasite’s parasitophorous vacuole membrane. Interference with the host cell Golgi-linked vesicular machinery using specific dominant-negative Arf and Rab GTPases results in developmental arrest and diminished survival of liver stage parasites. Moreover, functional Rab11a is critical for the parasites ability to induce Golgi fragmentation. Altogether, we demonstrate that the structural and functional integrity of the host cell Golgi is necessary for optimal pre-erythrocytic development of P. berghei. The parasite hijacks the hepatocyte’s Golgi structure to optimize its own intracellular development.


Author(s):  
Lakshmi Balasubramanian ◽  
Vanessa Zuzarte-Luís ◽  
Tabish Syed ◽  
Debakshi Mullick ◽  
Saptarathi Deb ◽  
...  

2007 ◽  
Vol 176 (3) ◽  
pp. 263-268 ◽  
Author(s):  
Adam C. Smith ◽  
Won Do Heo ◽  
Virginie Braun ◽  
Xiuju Jiang ◽  
Chloe Macrae ◽  
...  

Members of the Rab guanosine triphosphatase (GTPase) family are key regulators of membrane traffic. Here we examined the association of 48 Rabs with model phagosomes containing a non-invasive mutant of Salmonella enterica serovar Typhimurium (S. Typhimurium). This mutant traffics to lysosomes and allowed us to determine which Rabs localize to a maturing phagosome. In total, 18 Rabs associated with maturing phagosomes, each with its own kinetics of association. Dominant-negative mutants of Rab23 and 35 inhibited phagosome–lysosome fusion. A large number of Rab GTPases localized to wild-type Salmonella-containing vacuoles (SCVs), which do not fuse with lysosomes. However, some Rabs (8B, 13, 23, 32, and 35) were excluded from wild-type SCVs whereas others (5A, 5B, 5C, 7A, 11A, and 11B) were enriched on this compartment. Our studies demonstrate that a complex network of Rab GTPases controls endocytic progression to lysosomes and that this is modulated by S. Typhimurium to allow its intracellular growth.


2021 ◽  
pp. 112764
Author(s):  
Phulwanti Kumari Sharma ◽  
Inderjeet Kalia ◽  
Vibha Kaushik ◽  
Daniela Brünnert ◽  
Afshana Quadiri ◽  
...  

2013 ◽  
Vol 20 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Peter Liehl ◽  
Vanessa Zuzarte-Luís ◽  
Jennie Chan ◽  
Thomas Zillinger ◽  
Fernanda Baptista ◽  
...  

2005 ◽  
Vol 58 (3) ◽  
pp. 731-742 ◽  
Author(s):  
Claudia van de Sand ◽  
Sebastian Horstmann ◽  
Anja Schmidt ◽  
Angelika Sturm ◽  
Stefanie Bolte ◽  
...  

2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 106-107
Author(s):  
Alfredo Ulloa-Aguirre ◽  
Teresa Zariñán ◽  
Aída Uribe ◽  
Guadalupe Maya-Núñez ◽  
P. Michael Conn ◽  
...  

ACS Omega ◽  
2020 ◽  
Vol 5 (13) ◽  
pp. 7254-7261 ◽  
Author(s):  
Shahanavaj Khan ◽  
Sabika Zaidi ◽  
Abdulaziz Saleh Alouffi ◽  
Iftekhar Hassan ◽  
Ahmad Imran ◽  
...  

1980 ◽  
Vol 58 (11) ◽  
pp. 2018-2025 ◽  
Author(s):  
Bodo E. G. Mueller

Eimeria canadensis sporozoites were inoculated into monolayer cultures of Madin–Darby bovine kidney and primary bovine embryonic kidney cells. Sporozoites retained their shape for at least 9 days. At that time, the nucleus was enlarged and contained a prominent nucleolus, and amylopectin granules were no longer apparent. The width of the parasitophorous vacuole (pv) between host cell cytoplasm and parasite pellicle widened during transformation of sporozoites into multinucleate schizonts. Areas of altered host cell cytoplasm immediately adjacent to the pv membrane increased in size and became confluent, resulting in the formation of two distinct layers of cytoplasm. The outer zone contained the host cell nucleus, mitochondria, Golgi stacks, and ER, whereas the inner layer appeared granular and was void of all cell organelles except structures resembling ribosomes. Microfilaments were abundant at the border between inner and outer zone. In the most advanced stages observed, host cell organelles persisted only in the perinuclear region. The remaining, attenuated cytoplasm resembled the former inner zone.The novel ultrastructural observation of a bilayered cytoplasm of cells harbouring E. canadensis schizonts is compared with light microscope reports of similar effects caused by other Eimeria species of ruminants and with electron microscope findings of altered intestinal and abomasal cells of sheep harbouring "globidial" schizonts.


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