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S A Tolin

Publications and source records attributed to S A Tolin.

14 recordsLinked to original sources

Plant pathogen forensics: capabilities, needs, and recommendations.

A biological attack on U.S. crops, rangelands, or forests could reduce yield and quality, erode consumer confidence, affect economic health and the environment, and possibly impact human nutrition and international relations. Preparedness for a crop bioterror event requires a strong national security plan that includes steps for microbial forensics and criminal attribution. However, U.S. crop producers, consultants, and agricultural scientists have traditionally focused primarily on strategies for prevention and management of diseases introduced naturally or unintentionally rather than on responding appropriately to an intentional pathogen introduction. We assess currently available information, technologies, and resources that were developed originally to ensure plant health but also could be utilized for postintroduction plant pathogen forensics. Recommendations for prioritization of efforts and resource expenditures needed to enhance our plant pathogen forensics capabilities are presented.

Bioterrorism↗

Emergence of Rsv-resistance breaking Soybean mosaic virus isolates from Korean soybean cultivars.

Twelve Rsv resistance-breaking (RB) isolates of Soybean mosaic virus (SMV) were obtained from field-grown soybean plants showing mosaic symptoms and subsequently examined biologically and molecularly. All of these RB isolates were identified as SMV based on serological and infectivity assays, and the amplification of P1 gene products by reverse transcription-polymerase chain reaction (RT-PCR). Differential soybean cultivars, lines or accessions Lee 68 (rsv), PI 96983, York, Marshall, Ogden, Kwanggyo, Suweon 97 (Rsv1 alleles), L29 (Rsv3), and V94-5152 (Rsv4), following inoculation with each RB isolate, showed similar systemic symptoms suggesting that these RB isolates can overcome Rsv resistance at three loci. To differentiate the 12 RB isolates molecularly, the P1 coding region for each isolate was amplified, cloned, sequenced and compared to known SMV strains. The P1 region from the RB isolates shared 86-90% and 90-99% similarities in amino acid (aa) and nucleotide sequence, respectively, with known SMV strains. Comparison of aa sequences indicated that these RB isolates are newly emerging isolates capable of breaking Rsv resistance. Phylogenetic analysis further suggested that the RB isolates can be classified as three major types. However, recombination was not observed within the coding region of P1 protein among the types. This is the first report on the emergence of SMV isolates capable of overcoming all of the known resistance alleles at the Rsv1 locus, as well as distinct resistance genes at Rsv3 and Rsv4.

Amino Acid Sequence↗

Recombination within a nucleotide-binding-site/leucine-rich-repeat gene cluster produces new variants conditioning resistance to soybean mosaic virus in soybeans.

The soybean Rsv1 gene for resistance to soybean mosaic virus (SMV; Potyvirus) has previously been described as a single-locus multi-allelic gene mapping to molecular linkage group (MLG) F. Various Rsv1 alleles condition different responses to the seven (G1-G7) described strains of SMV, including extreme resistance, localized and systemic necrosis, and mosaic symptoms. We describe the cloning of a cluster of NBS-LRR resistance gene candidates from MLG F of the virus-resistant soybean line PI96983 and demonstrate that multiple genes within this cluster interact to condition unique responses to SMV strains. In addition to cloning 3gG2, a strong candidate for the major Rsv1 resistance gene from PI96983, we describe various unique resistant and necrotic reactions coincident with the presence or absence of other members of this gene cluster. Responses of recombinant lines from a high-resolution mapping population of PI96983 (resistant) x Lee 68 (susceptible) demonstrate that more than one gene in this region of the PI96983 chromosome conditions resistance and/or necrosis to SMV. In addition, the soybean cultivars Marshall and Ogden, which carry other previously described Rsv1 alleles, are shown to possess the 3gG2 gene in a NBS-LRR gene cluster background distinct from PI96983. These observations suggest that two or more related non-TIR-NBS-LRR gene products are likely involved in the allelic response of several Rsv1-containing lines to SMV.

Base Sequence↗

Inheritance and allelism tests of Raiden soybean for resistance to soybean mosaic virus.

The gene symbol Rsv2 was previously assigned to the gene in the soybean [Glycine max (L.) Merr.] line OX670 for resistance to soybean mosaic virus (SMV). The Rsv2 gene was reported to be derived from the Raiden soybean (PI 360844) and to be independent of Rsv1. Accumulated data from our genetic experiments were in disagreement with this conclusion. In this study, Raiden and L88-8431, a Williams BC5 isoline with SMV resistance derived from Raiden, were crossed with two SMV-susceptible cultivars to investigate the mode of inheritance of SMV resistance in Raiden. They were also crossed with five resistant cultivars to examine the allelomorphic relationships of the Raiden gene with other reported genes at the Rsv1 locus. F1 plants, F2 populations, and F2-derived F3 (F2:3) lines were tested with SMV strains G1 or G7 in the greenhouse or in the field. The individual plant reactions were classified as resistant (R, symptomless), necrotic (N, systemic necrosis), or susceptible (S, mosaic). The F2 populations from R x S crosses segregated in a ratio of 3 (R + N):1 S and the F2:3 lines from Lee 68 (S) x Raiden (R) exhibited a segregation pattern of 1 (all R):2 segregating:1 (all S). The F2 populations and F2:3 progenies from all R x R crosses did not show any segregation for susceptibility. These results demonstrate that the resistance to SMV in Raiden and L88-8431 is controlled by a single dominant gene and the gene is allelic to Rsv1. The heterozygous plants from R x S and R x N crosses exhibited systemic necrosis when inoculated with SMV G7, indicating a partial dominance nature of the resistance gene. Raiden and L88-8431 are both resistant to SMV G1-G4 and G7, but necrotic to G5, G6, and G7A. Since the resistance gene in Raiden is clearly an allele at the Rsv1 locus and it exhibits a unique reaction to the SMV strain groups, assignment of a new gene symbol, Rsv1-r, to replace Rsv2 would seem appropriate. Further research is ongoing to investigate the possible existence of the Rsv2 locus in OX670 and its relatives.

Crosses, Genetic↗

Complementary action of two independent dominant genes in Columbia soybean for resistance to Soybean mosaic virus.

A stem-tip necrosis disease was observed in the soybean [Glycine max (L.) Merr.] cultivar Columbia and its derivative OX686 when infected with a necrosis-causing strain of Soybean mosaic virus (SMV) in Canada. A dominant gene named Rsv3 was found in OX686 for the necrotic reaction. In the present research we have found that Columbia is resistant to all known SMV strains G1-G7, except G4. Genetic studies were conducted to investigate the inheritance of resistance in Columbia and interactions of resistance gene(s) with SMV strains. Columbia was crossed with a susceptible cultivar, Lee 68, and with resistant lines PI96983, Ogden, and LR1, each possessing a resistance gene at the Rsv1 locus. F(1) individuals, F(2) populations, and F(2:3) lines from these crosses were inoculated with G7 or G1 in the greenhouse. Our inheritance data confirmed the presence of two independent dominant genes for SMV resistance in Columbia. Results from allelism tests further demonstrate that the two genes (referred to as R3 and R4 in this article) in Columbia were independent of the Rsv1 locus. R3 appears to be the same gene previously reported as Rsv3 in OX686, which was derived from Columbia. The R3 gene confers resistance to G7, but necrosis to G1. The other gene, R4, conditions resistance to G1 and G7 at the early seedling stage and then a delayed mild mosaic reaction (late susceptible) 3 weeks later. Plants carrying both the R3 and R4 genes were completely resistant to both G1 and G7, indicating that the two genes interact in a complementary fashion. Plants heterozygous for R3 or R4 exhibited systemic necrosis or late susceptibility, suggesting that the resistance is allele dosage dependent. The R4 gene appeared epistatic to R3 since it masked expression of necrosis associated with the response of R3. The complementary interaction of two resistance genes, as exhibited in Columbia, can be useful in development of soybean cultivars with multiple and durable resistance to SMV.

Colombia↗

Inheritance and allelism of resistance to soybean mosaic virus in Zao18 soybean from China.

Soybean mosaic disease caused by soybean mosaic virus (SMV) occurs wherever soybean [Glycine max (L.) Merr.] is grown and is considered one of the most important soybean diseases in many areas of the world. Use of soybean cultivars with resistance to SMV is a very effective way of controlling the disease. China has rich soybean germplasm, but there is very limited information on genetics of SMV resistance in Chinese soybean germplasm and reaction of the resistance genes to SMV strains G1-G7. There also is no report on allelic relationships of resistance genes in Chinese soybeans with other named genes at the three identified loci Rsv1, Rsv3, and Rsv4. The objectives of this study were to examine reactions of Chinese soybean cultivar Zao18 to SMV strains G1-G3 and G5-G7, to reveal the inheritance of SMV resistance in Zao18 and to determine the allelic relationship of resistance genes in Zao18 with previously reported resistance genes. Zao18 was crossed with the SMV-susceptible cultivar Lee 68 to study the inheritance of resistance. Zao18 was also crossed with the resistant lines PI96983, L29, and V94-5152, which possess Rsv1, Rsv3, and Rsv4, respectively, to examine the allelic relationship between the genes in Zao18 and genes at these three loci. Our research results indicated that Zao18 possesses two independent dominant genes for SMV resistance, one of which is allelic to the Rsv3 locus; the other is allelic with Rsv1. The presence of both genes (Rsv1 and Rsv3) in Zao18 confers resistance to SMV strains G1-G7.

Alleles↗

Genetic study of a lethal necrosis to soybean mosaic virus in PI 507389 soybean.

PI 507389 soybean [Glycine max (L.) Merr.], a large-seeded line from Japan, exhibits a rapid, lethal, necrotic response to strains G1, G2, G5, and G6 of soybean mosaic virus (SMV). Unlike the hypersensitive necrotic reaction, this stem-tip necrosis can be a serious threat to soybean production. To investigate the genetic basis of lethal necrosis (LN), PI 507389 was crossed with the susceptible (S) cv. Lee 68 and with resistant (R) lines PI 96983, cv. York, and cv. Marshall, which carry single dominant genes for SMV resistance at the Rsv1 locus. F(1) plants, F(2) populations, and F(2:3) lines were inoculated with G1 and G6 in the greenhouse or in the field. Results indicated that LN is controlled by a single gene allelic to Rsv1, and this allele in PI 507389 is recessive to R alleles in PI 96983, York, and Marshall. The LN allele is codominant with the allele for S, for the heterozygotes showed a mixed phenotype of both necrosis (N) and mosaic (M) symptoms (NM). The LN allele becomes recessive to the S allele as the mixed NM shifts to S at a later stage in response to more virulent strains. The gene symbol Rsv1-n is assigned for the allele conferring LN in PI 507389. Rsv1-n is the only allele at the Rsv1 locus conditioning N to G1 and no R to any other SMV strains, and thus a unique genotype for SMV strain differentiation. The phenotypic expression of heterozygotes and the dominance relationships among R, N, and S depend on the virulence of SMV strains, source of alleles, and developmental stage.

Alleles↗

Genetics of resistance to two strains of soybean mosaic virus in differential soybean genotypes.

There are seven pathotypes of soybean mosaic virus (SMV) representing seven strain groups (G1-G7) in the United States. Soybean genotypes [Glycine max (L.) Merr.] may exhibit resistant (R), susceptible (S), or necrotic (N) reactions upon interacting with different SMV strains. This research was conducted to investigate whether reactions to two SMV strains are controlled by the same gene or by separate genes. Two SMV-resistant soybean lines, LR1 and LR2, were crossed with the susceptible cultivar Lee 68. LR1 contains a resistance gene Rsv1-s and is resistant to strains G1-G4 and G7. LR2 contains the Rsv4 gene and is resistant to strains G1-G7. Two hundred F(2:3) lines from LR1 x Lee 68 and 262 F(2:3) lines from LR2 x Lee 68 were screened for SMV reaction. Seeds from each F2 plant were randomly divided into two subsamples. A minimum of 20 seeds from each subsample were planted in the greenhouse and plants were inoculated with either G1 or G7. G1 is the least virulent, whereas G7 is the most virulent strain of SMV. The results showed that all the F(2:3) lines from both crosses exhibited the same reaction to G1 and G7. No recombinants were found in all the progenies for reactions to G1 and G7 in either cross. The results indicate that reactions to both G1 and G7 are controlled by either the same gene or very closely linked genes. This research finding is valuable for studying the resistance mechanism and interactions of soybean genotypes and SMV strains and for breeding SMV resistance to multiple strains.

Crosses, Genetic↗

Hemorrhagic enteritis of turkeys: electron microscopy of the causal virus.

Spleens of turkey poults inoculated with hemorrhagic enteritis virus were examined by electron microscopy. Negatively stained infectious extracts of spleen tissue contained adenolike virions averaging 75-80 nm in diameter. Intranuclear virions, either scattered or in crystalline arrays, were observed in thin sections of spleen tissue four days after inoculation. The chromatin was condensed and marginated in the nuclei of most cells which contained virions. Some virions in sections appeared as hollow cores with a double-layered capsid. The outer capsid was 75-80 nm in diameter, and the inner capsid 35-40 nm. Virions were not observed in cells or extracts of spleens from uninoculated poults. The detection of intranuclear virions at the time when symptoms appeared and specific antigen titer increased suggests that the adeno-like virions are the causal agent of hemorrhagic enteritis of turkeys.

Adenoviridae↗