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פותח על ידי קלירמאש פתרונות בע"מ -
TYLCV-Is movement in planta does not require V2 protein
Year:
2015
Source of publication :
Virology
Authors :
בלאוסוב, אדוארד
;
.
גפני, ידידיה
;
.
האק, חגית
;
.
לוי, יעל
;
.
לפידות, משה
;
.
צ'נדראן, סם
;
.
Volume :
477
Co-Authors:

Hak, H., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel, Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Israel
Levy, Y., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Chandran, S.A., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Belausov, E., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Loyter, A., Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Israel
Lapidot, M., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Gafni, Y., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel

Facilitators :
From page:
56
To page:
60
(
Total pages:
5
)
Abstract:
Tomato yellow leaf curl virus (TYLCV), a major tomato pathogen causing extensive crop losses, is a whitefly-transmitted geminivirus. V2 mutants of TYLCV-Is and related viruses tend to induce symptomless infection with attenuated viral DNA levels, while accumulating close to wild-type DNA levels in protoplasts, suggesting V2 as a movement protein. The discovery of plant-silencing mechanisms and viral silencing suppressors, V2 included, led us to reconsider V2's involvement in viral movement. We studied two mutant versions of the virus, one impaired in V2 silencing-suppression activity, and another carrying a non-translatable V2. While both mutant viruses spread in the infected plant to newly emerged leaves at the same rate as the wild-type virus, their DNA-accumulation levels were tenfold lower than in the wild-type virus. Thus, we suggest that the setback in virus proliferation, previously ascribed to a movement impediment, is due to lack of silencing-suppression activity. © 2015 Elsevier Inc.
Note:
Related Files :
Crop Production
gene silencing
Genetics
metabolism
Tomato yellow leaf curl virus
v2 protein
Virology
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/j.virol.2015.01.007
Article number:
0
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
27688
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:33
Scientific Publication
TYLCV-Is movement in planta does not require V2 protein
477

Hak, H., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel, Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Israel
Levy, Y., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Chandran, S.A., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Belausov, E., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Loyter, A., Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Israel
Lapidot, M., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel
Gafni, Y., Institute of Plant Sciences, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel

TYLCV-Is movement in planta does not require V2 protein
Tomato yellow leaf curl virus (TYLCV), a major tomato pathogen causing extensive crop losses, is a whitefly-transmitted geminivirus. V2 mutants of TYLCV-Is and related viruses tend to induce symptomless infection with attenuated viral DNA levels, while accumulating close to wild-type DNA levels in protoplasts, suggesting V2 as a movement protein. The discovery of plant-silencing mechanisms and viral silencing suppressors, V2 included, led us to reconsider V2's involvement in viral movement. We studied two mutant versions of the virus, one impaired in V2 silencing-suppression activity, and another carrying a non-translatable V2. While both mutant viruses spread in the infected plant to newly emerged leaves at the same rate as the wild-type virus, their DNA-accumulation levels were tenfold lower than in the wild-type virus. Thus, we suggest that the setback in virus proliferation, previously ascribed to a movement impediment, is due to lack of silencing-suppression activity. © 2015 Elsevier Inc.
Scientific Publication
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