July
1999
, Volume
89
, Number
7
Pages
540
-
545
Authors
R. G.
Guevara-González
,
P. L.
Ramos
,
and
R. F.
Rivera-Bustamante
Affiliations
Departamento de Ingeniería Genética, Centro de Investigación y de Estudios Avanzados del IPN, Unidad Irapuato, Apartado Postal 629, Irapuato, Gto. México
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RelatedArticle
Accepted for publication 12 April 1999.
Abstract
ABSTRACT
The role of the pepper huasteco virus (PHV) coat protein (CP) gene during the infection was investigated in three different hosts by using mutations that produced truncated proteins and by complementation assays in transgenic plants. The infectivity analysis revealed that mutants that express truncated CP (CP7 and CP191) behave like the wild-type virus when inoculated onto pepper and Nicotiana benthamiana plants in terms of symptom expression and viral DNA movement. On the contrary, the CP7 mutant was unable to systemically infect tobacco plants, whereas only 10% of the plants inoculated with the CP191 mutant became infected. The CP7 mutant was complemented by coinoculating it with another geminivirus (taino tomato mottle virus). No complementation was observed in plants from nine transgenic tobacco lines expressing CP under the control of the cauliflower mosaic virus (CaMV) 35S promoter. However, 3 out of 10 lines expressing CP under the control of its own promoter (693 nucleotides) were able to complement the CP7 mutant. Interestingly, upon infection, the levels of CP mRNA in 693CP plants increased dramatically, probably due to transactivation of the CP promoter by the viral protein AC2.
JnArticleKeywords
Additional keywords:
geminivirus promoter,
AC2 transactivation.
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ArticleCopyright
© 1999 The American Phytopathological Society