Differential Transmission of Triticum mosaic virus by Wheat Curl MitePopulations Collected in the Great Plains

McMechan, A. J., Tatineni, S., French, R., and Hein, G. L. 2014. Differential transmission of Triticum mosaic virus by wheat curl mite populations collected in the Great Plains. Plant Dis. 98:806-810. Wheat is an important food grain worldwide and the primary dryland crop in the western Great Plains. A complex of three wheat curl mite (WCM)-transmitted viruses (Wheat streak mosaic virus, High plains virus, and Triticum mosaic virus [TriMV]) is a cause of serious loss in winter wheat production in the Great Plains. TriMV was first reported in Kansas in 2006 and later found in most other Great Plains states. Currently, three populations of WCM have been identified by genetic characterization and differential responses to mite resistance genes in wheat. In this study, we examined TriMV transmission by these three WCM populations: ‘Nebraska’ (NE), ‘Montana’ (MT), and ‘South Dakota’ (SD). Mite transmission using single-mite transfers revealed that the NE WCM population transmitted TriMV at 41%, while the MT and SD WCM populations failed to transmit TriMV. In multi-mite transfers, the NE WCM population transmitted TriMV at 100% level compared with 2.5% transmission by MT and SD WCM populations. Interestingly, NE mites transferred during the quiescent stages following the first and second instar transmitted TriMV at a 39 to 40% rate, suggesting that immature mites were able to acquire the virus and maintain it through molting. In addition, mite survival for single-mite transfers was significantly lower for NE mites when transferred from TriMV-inoculated source plants (60%) compared with mockinoculated source plants (84%). This demonstrates potentially negative effects on WCM survival from TriMV. TriMV transmission differences demonstrated in this study underscore the importance of identification of mite genotypes for future studies with TriMV. The wheat-mite–virus complex is an important production constraint to winter wheat in the western Great Plains. Average annual losses associated with Wheat streak mosaic virus (WSMV) are estimated at 1% (1); however, localized yield losses approaching 100% are not uncommon. The wheat curl mite (WCM), Aceria tosichella Keifer, is the only known vector of the three viruses that make up this wheat-mite–virus complex: WSMV, High plains virus (HPV), and Triticum mosaic virus (TriMV). WSMV was identified in 1922 as “yellow mosaic”, and it is the best understood of the viruses within this complex (23). HPV was identified in the 1990s, and it has been difficult to study because it is not mechanically transmissible (12). TriMV was recently identified in wheat in Kansas in 2006 (20) and later found across most Great Plains states (2,3). To reduce the impact of the wheat-mite–virus complex, wheat varieties have been developed with resistance to both the mite and the viruses they transmit. ‘TAM 107’ wheat was the first commercial variety released in the late-1980s with resistance to WCM colonization (17,27). The popularity and widespread distribution of this variety led to the development of WCM populations adapted to this mite resistant cultivar (8,9). In addition, Harvey et al. (10) found differences in survival of different WCM collections on resistant varieties with different mite resistance genes. Carew et al. (5) identified two distinct lineages of WCM (types 1 and 2) in Australia based on a mitochondrial 16S ribosomal DNA (rDNA) gene and two nuclear markers. Schiffer et al. (16) tested the Australian mite types for transmission of WSMV and determined that only one type was able to transmit the virus. Hein et al. (11) tested the five mite populations used by Harvey et al. (10) for genetic diversity using polymerase chain reaction (PCR) restriction fragment length polymorphism of mitochondrial and rDNA. Results indicated two distinct mite genotypes similar to Carew et al. (5) mite types. The ‘Nebraska’ (NE) population (type 2) was genetically distinct from the remaining populations: ‘Kansas’ (KS), ‘Montana’ (MT), ‘South Dakota’ (SD), and ‘Texas’ (TX) (type 1). Slight differences were observed between MT and other type 1 populations. The magnitude of differences between these type 1 and type 2 WCMs was comparable with the differences between A. tosichella and the dry bulb mite, A. tulipae Keifer. However, North American mite types were found to have no significant differences in transmission of WSMV (18). Seifers et al. (18) observed significant differences in transmission of HPV between these North American mite populations. The NE population was shown to be a much better transmitter of HPV than the other mites but the transmission rate for the MT population increased when doubly infected with WSMV (18). The complete life cycle of the WCM requires 7 to 10 days, with an egg, larva, nymph, and adult stage (23). Just prior to each molt there is a nonfeeding quiescent phase lasting about 18 h where the mites remain inactive and appear partially translucent (23). WSMV is transmitted by all active stages of the WCM (6,14,15,21,22). Within 15 min of feeding, 1% of WCMs are capable of acquiring WSMV and longer acquisition times increased the transmission rate. WCM can transmit WSMV for up to 7 days after acquisition at room temperature (23 to 28°C) and up to 61 days at 3°C (14). Adult WCMs are unable to acquire WSMV but they can transmit the virus if it is acquired during earlier stages of development. Adults were less efficient vectors of WSMV when compared with immature mites (14). In another study, transferring quiescent WCMs from WSMV-inoculated plants resulted in a 94% transmission rate (21). TriMV is a plus-sense, single-stranded RNA virus consisting of 10,266 nucleotides with a polyprotein of 3,112 amino acids, and it Corresponding author: A. J. McMechan, E-mail: [email protected] The findings and conclusions in this article do not necessarily reflect the view of the United States Department of Agriculture. Accepted for publication 21 December 2013. http://dx.doi.org/10.1094/PDIS-06-13-0582-RE © 2014 The American Phytopathological Society