Intracellular and Intercellular Transport of Viroids

Author(s):  
Biao Ding ◽  
Asuka Itaya
2000 ◽  
Vol 74 (23) ◽  
pp. 11339-11346 ◽  
Author(s):  
Vitaly Boyko ◽  
Jessica van der Laak ◽  
Jacqueline Ferralli ◽  
Elena Suslova ◽  
Myoung-Ok Kwon ◽  
...  

ABSTRACT Intercellular transport of tobacco mosaic virus (TMV) RNA involves the accumulation of virus-encoded movement protein (MP) in plasmodesmata (Pd), in endoplasmic reticulum (ER)-derived inclusion bodies, and on microtubules. The functional significance of these interactions in viral RNA (vRNA) movement was tested in planta and in protoplasts with TMV derivatives expressing N- and C-terminal deletion mutants of MP fused to the green fluorescent protein. Deletion of 55 amino acids from the C terminus of MP did not interfere with the vRNA transport function of MP:GFP but abolished its accumulation in inclusion bodies, indicating that accumulation of MP at these ER-derived sites is not a requirement for function in vRNA intercellular movement. Deletion of 66 amino acids from the C terminus of MP inactivated the protein, and viral infection occurred only upon complementation in plants transgenic for MP. The functional deficiency of the mutant protein correlated with its inability to associate with microtubules and, independently, with its absence from Pd at the leading edge of infection. Inactivation of MP by N-terminal deletions was correlated with the inability of the protein to target Pd throughout the infection site, whereas its associations with microtubules and inclusion bodies were unaffected. The observations support a role of MP-interacting microtubules in TMV RNA movement and indicate that MP targets microtubules and Pd by independent mechanisms. Moreover, accumulation of MP in Pd late in infection is insufficient to support viral movement, confirming that intercellular transport of vRNA relies on the presence of MP in Pd at the leading edge of infection.


2002 ◽  
Vol 9 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Lars Zender ◽  
Florian Kühnel ◽  
Reiner Köck ◽  
Michael Manns ◽  
Stefan Kubicka

Small ◽  
2016 ◽  
Vol 12 (14) ◽  
pp. 1882-1890 ◽  
Author(s):  
Markus Rehberg ◽  
Katharina Nekolla ◽  
Sabine Sellner ◽  
Marc Praetner ◽  
Karina Mildner ◽  
...  

Plasmodesmata ◽  
2007 ◽  
pp. 241-262 ◽  
Author(s):  
Karl Oparka ◽  
Petra Boevink

2013 ◽  
Vol 41 (1) ◽  
pp. 293-298 ◽  
Author(s):  
Samireh Jorfi ◽  
Jameel M. Inal

Microvesicles are shed constitutively, or upon activation, from both normal and malignant cells. The process is dependent on an increase in cytosolic Ca2+, which activates different enzymes, resulting in depolymerization of the actin cytoskeleton and release of the vesicles. Drug resistance can be defined as the ability of cancer cells to survive exposure to a wide range of anti-cancer drugs, and anti-tumour chemotherapeutic treatments are often impaired by innate or acquired MDR (multidrug resistance). Microvesicles released upon chemotherapeutic agents prevent the drugs from reaching their targets and also mediate intercellular transport of MDR proteins.


1991 ◽  
Vol 42 (11) ◽  
pp. 1393-1398 ◽  
Author(s):  
D. Q. DING ◽  
S. AMINO ◽  
T. NAGATA ◽  
M. TAZAWA

2011 ◽  
Vol 62 (15) ◽  
pp. 5249-5266 ◽  
Author(s):  
R. G. White ◽  
D. A. Barton

2009 ◽  
Vol 106 (9) ◽  
pp. 3615-3620 ◽  
Author(s):  
Y. Benitez-Alfonso ◽  
M. Cilia ◽  
A. S. Roman ◽  
C. Thomas ◽  
A. Maule ◽  
...  

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