الفهرس 
AbstractOnly 14 pages are availabe for public view
 |  | from | 188 |  |  |
| | | from | 188 | | |
Abstract
Plant diseases, particularly viruses, have a detrimental effect on agricultural productivity worldwide. In order to combat diseases, plants have developed sophisticated immune systems. The best method for combating plant viruses is to physically separate the pathogen from the host to prevent infection or to apply genetic resistance to stop or reduce the spread of the illness. Experiments were carried out to investigate the phenotypic, genotypic responses of different commercial selected soybean cultivars to SMV infection in Egypt and to evaluate the resistance components and defense genes of the cultivars through screening by Indirect-ELISA, RNA extraction, cDNA synthesis, traditional PCR, quantitative real-time PCR along side statistiical analysis . The different soybean genotypes displayed different responses to SMV strains. The symptoms of SMV infection and the viral concentration were assessed utilizing an ELISA assay in eight different Egyptian soybean cultivars (Giza 21, Giza 22, Giza 35, Giza 82, Giza 111, Crawford, H4L4, and PI416937). The ELISA results indicated that Giza 21 and Giza 35 were moderately resistant/ tolerant to SMV infection, while Giza 82 was the least resistant cultivar. Giza 22, Giza 111, and PI416937 were less resistant; however, H4L4 and Crawford were identified as the most resistant cultivars against SMV infection. The chi-square analysis showed a significant association between genotypes and response to SMV infection. The PCR test showed the presence of RSV1 (3gG2), RSV1 (5gG3), and RSV3 loci, and the absence of the RSV4 loci gene. The expression analysis of the selected defense genes (EDS1 , PAD4, EDR1, ERF1, and JAR1) showed variations in the fold changes between infected and non-infected soybean cultivars, demonstrating that these genes may be extremely important in this pathosystem. Additionally, there was a strong positive association between the expression levels of EDR1 and ERF genes.