|Kaiser Jr, Walter|
Submitted to: Plant Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/22/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Chickpeas are an important minor crop in Washington State and are currently restricted to the climactic region of the Palouse in the eastern section of the state. In the growing season of 1994, red clover vein mosaic virus (RCVMV-ChP) was isolated from chickpea growing in this section of Washington. Symptoms on chickpea included a mosaic in the leaves, malformation of leaves and branches, and severe stunting of the entire plant. Flower and pod formations were severely reduced, therefore, yield loss potential could be significant. The virus could be differentiated from the type strain originally from pea (RCVMV-110, ATCC) by mechanical inoculation to host plants Chenopodium amaranticolor and C. Quinoa. An additional host of potential economic importance, lentil (Lens culinaris L.), was determined also to be a host of RCVMV-ChP. Lentil has not been reported as a host for RCVMV. 'Puget' peas (Pisum sativum L.) were mechanically inoculated with RCVMV-ChP and RCVMV-110 respectively, and see collected from infected plants. None (0/31) of the RCVMV-ChP seedlings tested positive for the virus, while 3.7% of the RCVMV-110 seedlings were infected. Studies by ELISA and western blots indicated no serological relationships between RCVMV-ChP and two other carlaviruses, pea streak virus or alfalfa latent virus. Pea streak virus has previously been the only carlavirus to occur in chickpea. This is the first report of RCVMV infecting the experimental host lentil and naturally occurring in chickpea.
Technical Abstract: Chickpeas (Cicer arietinum L.) are an important minor legume crop grown in eastern Washington State. During the growing season of 1994, a naturally occurring strain of red clover vein mosaic carlavirus (RCVMV-ChP) was isolated from chickpea grown in the Palouse region of the state. Symptoms included severe stunting, mosaic, proliferation of axillary buds, and malformation of leaves and branches. Flower and pod formations were severely reduced. The virus could be differentiated from the type strain (RCVMV pv110, ATCC) by mechanical inoculation to Chenopodium amaranticolor and C. quinoa. RCMV-ChP produced chlorotic local lesions on inoculated leaves while RCVMV 110 produced necrotic local lesions. An additional host of RCVMV-ChP was lentil (Lens culinaris L.). Lentil has not been reported as a host for RCVMV. Seed transmission experiments were performed by mechanically inoculating 'Puget' pea (Pisum sativum L.) followed by collection of progeny seed. Seedlings were tested for RCMV using indirect ELISA 10 days after emergence. None (0/31) of the RCVMV-ChP seedlings tested positive for the virus, while 3.7% (1/27) of the RCVMV-110 seedlings were infected. Purified virions of RCVMV-ChP revealed a capsid protein molecular weight of ca. 32000 Daltons when determined by SDS-Page and western blots. The virion nucleic acid consisted of a single species ssRNA with a molecular weight of 7.05 x 10**6. Studies by ELISA and western blots indicated no serological relationship between RCVMV-ChP and isolates of pea streak or alfalfa latent carlaviruses, but was indistinguishable from RCVMV-110. Pea streak virus previously has been the only carlavirus reported to occur in chickpea. This is the first report of RCVMV infecting the experimental host lentil and naturally occurring in chickpea.