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Stewart Gray
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Stewart M. Gray
Research Plant Pathologist, USDA, ARS, BioIPM

Courtesy Professor, Department of Plant Pathology
Cornell University

(607) 255-7844 (Voice)
(607) 255-2459 (FAX)



Ph.D. North Carolina State University, 1987
MS North Carolina State University, 1984
BS Southampton College, 1979
Professional Experience

1989 -

1987 - 93
1993 - 01
2001 -
1993 - 02

2002 -        

Research Plant Pathologist, USDA, ARS, Biological Integrated Pest Management Research Unit
Assistant Professor, Cornell University, Department of Plant Pathology
Associate Professor, Cornell University, Department of Plant Pathology
Professor, Cornell University, Department of Plant Pathology
Adjunct Assistant Professor, Pennsylvania State University,
Department of Plant Pathology
Adjunct Professor, Pennsylvania State University, Department of Plant

Research Interests
My research program focuses on virus diseases of potato and small grain crops. A major emphasis is to develop an understanding of the relationships between plant viruses and their insect vectors. A second area is the management of plant virus diseases based on a sound understanding of how virus-insect vector-plant host relationships affect the epidemiology and ecology of the disease.
The research on the fundamental relationships between insects and viruses currently focuses on members of the Luteoviridae and their aphid vectors. The luteovirids are vectored specifically by different species of aphids. One research thrust is to understand the cellular and molecular mechanisms that determine the vector specific transmission. A working hypothesis is that virus-vector specificity involves an interaction between viral capsid proteins and membrane receptors on the aphid hindgut and salivary gland. Both the major capsid protein and the minor readthrough capsid protein play a role in transport of virus across gut and salivary tissues. These proteins also partially regulate the movement and accumulation of virus in plant hosts.
The aphid also plays an important part in the regulation of virus transmission. Several genotypes within the aphid,  , were identified that differ in their ability to transmit one or more species of virus causing barley yellow dwarf disease. Sexual forms of a competent vector and of a nonvector were  induced and crossed to generate F1 and F2 aphid populations that are segregating for transmission phenotypes in a virus species dependent manner. Transmission of different virus species is regulated by an overlapping but distinct set of genes that are inherited in an additive manner. The genes regulating virus transport across gut and salivary tissues are not linked and hemolymph associated factors are not involved in virus transmission in this system. Genomic and proteomic approaches have correlated the presence or absence of specific genes and proteins with a transmission phenotype.
In recent years, Potato Virus Y (PVY) has re-emerged as a serious disease problem in many seed potato production areas in the United States. High levels of PVY means fewer certified seed lots, loss of farm income, and increased initial PVY inoculum levels in the next years commercial crop. Our research has shown that potato cultivars differ not only in the percentage of tubers that become infected, but also in the rate that those infected tubers sprout and give rise to infected plants. An inefficient infection of progeny tubers coupled with reduced sprouting of infected tubers would contribute fewer infected plants; virus incidence in that variety would become somewhat self-limiting especially in successive cropping years with minimal aphid vector activity.  By contrast, the percentage of infected seed pieces would increase in varieties that efficiently transmit PVY to progeny tubers that subsequently sprout vigorous infected plants attractive to aphid vectors. Thus, the management of PVY would not necessarily be the same for all varieties. 
        Not only is the incidence of the common strain of PVY (PVYO) increasing, but necrotic strains of PVY (PVYN, NTN) once thought to be excluded from U.S. have been identified in many production areas. Furthermore, the once distinct strain groupings are becoming blurred due to genetic changes (recombination and mutation) in the virus. Current diagnostic tests have not provided an accurate picture of specific PVY strain incidence and seed certification programs have been unable to limit the spread of the particularly damaging necrotic strains. Our recent surveys indicate a widespread increase in the incidence of necrotic strains, many of which are detrimental to tuber quality. There is limited information on why the necrotic strains have become more widespread, but, our  data  suggests that one contributing factor is the necrotic strains are more efficient at infecting tubers than the PVYO strain. Similar to the argument made above that varieties will differ in their overall contribution to PVY incidence, PVY strain is likely to be another important variable to consider. Depending upon the predominant PVY strain(s) present and its ability to infect tubers, a uniformly applied management policy may overestimate or underestimate the potential contribution to seed borne inoculum depending on how well the PVY strain is translocated to tubers and subsequently into the developing sprouts.

Publications Past 5 years

Gray, S. M., Smith, D. M., Barbieri, L. and Burd. J. D. 2002. Virus transmission phenotype is correlated with host adaptation among genetically diverse populations of the aphid, Schizaphis graminum. Phytopathology 92: 970-975

Koenig, R., Bergstrom, G. C. and Gray, S. M. 2002. A New York isolate of Soil-borne wheat mosaic virus differs from the Nebraska type isolate in the nucleotide sequence of coding regions, but not in the deduced amino acid sequence. Arch. Virol. 147:617-625

Lee, L., Palukaitis, P., Gray, S.M. 2002. Host-dependent requirement for the Potato leafroll virus 17-kDa protein in virus movement. MPMI 15:1086-1094

Carroll, J.E., Bergstrom, G.C., Gray, S.M. 2002. Assessing the resistance of winter wheat to wheat spindle streak mosaic bymovirus. Can. J. Pl. Path. 24:465-470

Gray, S.M. and Gildow, F.E. 2003. Luteovirus-Aphid interactions. Ann. Rev. Phytopathology. 41:539-566.

Cadle-Davidson, L., Schindelbech, R. R., van Es, H. M., Gray, S. M., and Bergstrom, G. C. 2003. Using air pressure cells to evaluate the effect of soil environment on the transmission of soilborne viruses of wheat. Phytopathology. 93:1131-1136.

Liang, D., Gray, S. M., Kaplan, I., and Palukaitis, P. 2004. Site-directed mutagenesis and generation of chimeric viruses by homologous recombination in yeast to facilitate analysis of plant-virus interactions. MPMI. 17:571-576.

Lee, L., Kaplan, I. B., Ripoll, D. R., Liang, D., Palukaitis, P., Gray, S. M. 2005. A surface loop of the potato leafroll virus coat protein is involved in virion assembly and aphid transmission. J. Virology 79:1207-1214

Cadle-Davidson, L. and Gray, S.M. 2006. Soil-borne wheat mosaic virus. The Plant Health Instructor. DOI: 10.1094/PHI-I-2006-0424-01.

Baldauf, P.M., Gray, S.M., and Perry, K.L. 2006. Biological and serological properties of Potato virus Y isolates in Northeastern United States potato. Plant Dis. 90:559-566.

Ali, A., Li, H., Schneider, W.L., Sherman, D.J., Gray, S.M., Smith, D.M., and Roossinck, M.J. 2006. Analysis of genetic bottlenecks during horizontal transmission of Cucumber mosaic virus. J. Virol.

Cadle-Davidson, L., Sorrells, M.E., Gray, S.M., and Bergstrom, G.C. 2006. Identification of small grains genotypes resistant to soilborne wheat mosaic virus. Plant Disease 90:1039-1044.

Cadle-Davidson, L., Sorrells, M.E., Gray, S.M., and Bergstrom, G.C. 2006. Identification of small grains genotypes resistant to wheat spindle streak mosaic virus. Plant Disease 90:1045-1050

Burrows, M., Caillaud, M., Smith D., Benson, E., Gildow, F., and Gray, S.M. 2006. Genetic regulation of polerovirus and luteovirus transmission in the aphid Schizaphis graminum. Phytopathology 96: 828-837.

Burrows, M.E., Caillaud, M.C., Smith, D.M., and Gray, S.M. 2007. Biometrical genetic analysis of luteovirus transmission in the aphid, Schizaphis graminum. Heredity 98:106-113

Gray, S. M., Caillaud, M., Burrows, M., Smith, D. 2007. Transmission of viruses that cause barley yellow dwarf is controlled by different loci in the aphid, Schizaphis graminum. 2006. Insect Sci. 7: article 5.

Kaplan, I. B., Lee, L., Ripoll, D. R., Palukaitis, P., Gildow, F. E., and Gray, S. M. 2007.  Point mutations in the potato leafroll virus major capsid protein alter virion stability and aphid transmission. J. Gen. Virol. 88:1821-1830

Gray, S.M. 2007. Barley yellow dwarf. In, Compendium of Wheat Diseases, W.W.Bockus, ed. APS Press.
Liu, F., Wang, X., Liu, Y., Xie, J., Gray, S. M., Zhou, G., and Gao, B. 2007. A Chinese isolate of barley yellow dwarf virus-PAV represents a third distinct species within the PAV serotype. Arch. Virol. 152: 1365-1373