Effects of Single and Double Infections of Winter Wheatby Triticum mosaic virus and Wheat streak mosaic virus on Yield Determinants

نویسندگان

  • E. Byamukama
  • S. Tatineni
  • G. L. Hein
  • R. A. Graybosch
  • Stephen Baenziger
  • S. N. Wegulo
چکیده

Byamukama, E., Tatineni, S., Hein, G. L., Graybosch, R. A., Baenziger, P. S., French, R., and Wegulo, S. N. 2012. Effects of single and double infections of winter wheat by Triticum mosaic virus and Wheat streak mosaic virus on yield determinants. Plant Dis. 96:859-864. Triticum mosaic virus (TriMV) is a recently discovered virus infecting wheat (Triticum aestivum) in the Great Plains region of the United States. It is transmitted by wheat curl mites (Aceria tosichella) which also transmit Wheat streak mosaic virus (WSMV) and Wheat mosaic virus. In a greenhouse study, winter wheat ‘Millennium’ (WSMV susceptible) and ‘Mace’ (WSMV resistant) were mechanically inoculated with TriMV, WSMV, TriMV+WSMV, or sterile water at the two-leaf growth stage. At 28 days after inoculation, final chlorophyll meter (soil plant analysis development [SPAD]) readings, area under the SPAD progress curve (AUSPC), the number of tillers per plant, shoot and root weight, and total nitrogen and carbon content were determined. In Millennium, all measured variables were significantly reduced by single or double virus infections, with the greatest reductions occurring in the double-infection treatment. In Mace, only final SPAD readings, AUSPC, and total nitrogen were significantly reduced by single or double virus infections. There was a significant (P ≤ 0.05), positive linear relationship between SPAD readings and shoot weight in Millennium but not in Mace. The relationship between total nitrogen and shoot weight was positive, linear, and significant in both cultivars. The results from this study indicate that Mace, a WSMV-resistant cultivar, is also resistant to TriMV, and double infection of winter wheat by TriMV and WSMV exacerbates symptom expression and loss of biomass in susceptible cultivars. Triticum mosaic virus (TriMV) (genus Poacevirus, family Potyviridae) is a newly discovered virus that infects winter wheat (Triticum aestivum L.) in the Great Plains region of the United States (5,29). Since the first report in Kansas in 2006, TriMV has been found in Nebraska, South Dakota, Montana, Colorado, Texas, Wyoming, and Oklahoma (5; M. Burrows, unpublished data). TriMV has been found infecting wheat alone or in combination with Wheat streak mosaic virus (WSMV) (Tritimovirus, Potyviridae) and Wheat mosaic virus (WMoV)/High Plains Virus (HPV) (unassigned, Bunyaviridae) (5,27). All three viruses are transmitted by wheat curl mites (WCM; Aceria tosichella Keifer) and are among many viruses reported to infect wheat in the central Great Plains (28,29). Seifers et al. (26) and Tatineni et al. (33) showed that the host range of TriMV included barley (Hordeum vulgare L.), oat (Avena sativa L.), rye (Secale cereale L.), triticale (X. Triticosecale Wittmact), and several grass species. TriMV is a single-stranded positive-sense RNA virus with one open reading frame that encodes a polyprotein of 352 kDa (34). The complete genome sequence distinctively showed TriMV to belong to the family Potyviridae and to have 47 to 65% amino acid sequence similarity with Sugarcane streak mosaic virus (Poacevirus, Potyviridae) (34). TriMV infection elicits cultivarspecific symptoms that include systemic chlorotic streaks, mosaic, and mottling (33). Chlorotic streak and mottling symptoms indicate depletion of chlorophyll. TriMV co-infects wheat with WSMV synergistically, leading to enhanced symptom expression and increased titer of both viruses in susceptible wheat cultivars (33). WSMV is by far the most prevalent and the most economically important virus infecting winter wheat in the Great Plains region of the United States (5,31,32,37,39). Management of WSMV is mainly through removal of volunteer wheat and other alternative weed hosts which act as a “green bridge” for viruliferous WCM between the summer-harvested and fall-sown winter wheat crops (5). Another WSMV management strategy is the use of host resistance. Only a few winter wheat cultivars with highly effective resistance to WSMV are available (8,11,22) and some wheat lines with resistance to the disease have recently been identified (20,30). Cultivars with moderate resistance to WSMV have not been reported. With the discovery of TriMV and the fact that both WSMV and TriMV are transmitted by the same vector, there is a need to reevaluate resistance to WSMV when wheat is co-infected with both viruses. Lommel et al. (19) showed that, in winter wheat, resistance to Wheat soilborne mosaic virus (Furovirus, Virgaviridae) broke down in the presence of Wheat spindle streak mosaic virus (Bymovirus, Potyviridae) infection, indicating that the presence of a second virus in a host can cause resistance to the first virus to be ineffective. The number of fertile tillers (tillers with spikes) is an important yield determinant in winter wheat (4). Few studies have reported the effect of virus infection on tillers in winter wheat and other virus host crops (14–17). Larsen et al. (17) found no significant effect of WSMV infection on the number of tillers at 21 days after inoculation (DAI). Hunger et al. (14) reported up to 75% reduction in fertile tillers for seven winter wheat cultivars inoculated with WSMV in the fall. Shahwan and Hill (31) reported up to 93% reduction in fertile tillers when eight winter and four spring wheat cultivars were inoculated with WSMV in the greenhouse. Information is lacking on the effect of TriMV infection of wheat alone or in combination with WSMV on yield determinants such as number of tillers and plant biomass. Such information can be used to predict the expected yield loss when wheat is co-infected by both viruses. This information can, in turn, enable producers Corresponding author: S. N. Wegulo, E-mail: [email protected] The findings and conclusions in this article do not necessarily reflect the view of United States Department of Agriculture. Accepted for publication 13 January 2012. http://dx.doi.org/10.1094 / PDIS-11-11-0957-RE © 2012 The American Phytopathological Society

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تاریخ انتشار 2016