Prospects for the use of the tomato genetic collection of the FSBSI ARRIBPP to develop varieties with group resistance to Alternaria sp. and Phytophthora infestans (Mont.) de Bary

The resistance of mutant tomato lines to the main diseases upon the provocative infectious background was assessed. We used as experimental material 22 lines of the tomato genetic collection of the FSBSI ARRIBPP, Krasnodar. According to the results of assessing the damage by Alternaria sp. in the field it was found that line 41 exhibitted high resistance, there were no signs of disease damage. Mutant lines 80, 387, 434, 568, 620 showed resistance, the degree of the disease development varied within 1–8 %. Lines 172, 467, 509, 518 with a degree of development of 12–23 % were characterized by semi-resistance. Lines 41, 387 showed high resistance to P. infestans. No visible signs of damage by P. infestans were detected in these genotypes. Lines 341, 509, 518, 568 had semi-resistance to the pathogen, the degree of development varied from 10 to 18 %. The genotypes Mo 41 and 387 that showed high and relatively high resistance to Alternaria sp. and P. infestans are of the greatest interest for breeding and genetic work as sources of group resistance.


Introduction
Tomato is the most popular fruit crop in the world due to its wide range of use, nutritional value and unique taste [1][2]. However, biotic and abiotic factors hinder the commercial production of this culture when grown in open ground [3].
Among the biotic factors that can lead to significant yield losses of tomato crops, the most dangerous and harmful are fungi of the genus Alternaria sp. and oomycete Phytophthora infestans (Mont.) de Bary.
Recently, Alternaria sp. has become a leader in harmfulness among fungal diseases [4][5][6]. Damages of tomato plants caused by Alternaria sp. lead to yield losses, mold of seeds and fruits, and the metabolites of the fungus cause allergic reactions [7].
For many years, P. infestans oomycete has been recognized as the most dangerous pathogen in Russia, which reduces tomato yield up to 50 %, and in epiphytotic years up to 80 % or more [8][9][10][11][12][13]. Under the pathogen effect, the assimilation surface of tomato plants leaves decreases, fruits rot. The greatest damage was noted with increased humidity in open ground and in plastic-covered unheated greenhouses [14].
Cultivated tomato has a narrow genetic diversity, which was the result of its intensive selection and inbreeding during evolution. As a result, cultivated tomato species are more susceptible to disease than wild species and mutant forms. Thus, yield losses caused by pathogenic infections can be eliminated by developing resistant varieties with the help of plant breeding methods using the resistance genes of wild species and mutant forms of tomato [15][16][17][18].
To develop resistant varieties, breeders need tomato genetic collections with identified genes. One of such collections is supported at the FSBSI ARRIBPP, Krasnodar, where we comprehensively study the collection and select parent material for practical use in realizing the tasks of private selection [19].
Marker selection of the initial forms of tomato is a relatively new approach in breeding, which is based on the direct selection of plants by genes that determine economically valuable characteristics. As a result, the analysis of breeding material is carried out in a short time and most of the studied mutant forms can serve as a source of important economically valuable properties [20][21][22][23].
The aim of the study is to assess the resistance of mutant samples of the tomato genetic collection of the FSBSI ARRIBPP to diseases upon a provocative infectious background.

Materials and methods
As an experimental material, we used 22 samples from the collection of tomato mutant forms of the laboratory of the tomato genetic collection of the FSBSI ARRIBPP, Krasnodar (Table 1). Screening of 22 test mutant tomato lines for resistance to Alternaria sp. and P. infestans was carried out in the field of FSBSI ARRIBPP in 2019 upon the provocative infectious background created as a result of the repeated cultivation in one place for three years, without the use of plant protection products, with plant residues embedded in the soil. Plants were placed in randomized blocks with three replications. Each replication included 10 plants of each genotype. Sowing pattern: 1.5 m × 0.75 m. There were no chemical treatments. Recording of diseases was carried out with the appearance of the first signs of the disease. Resistance of mutant lines to Alternaria sp. and P. infestans was assessed by the degree of damage according to the modified method [24][25]. Meteorological conditions of 2019 vegetation period were favorable for the growth and development of tomato. In July, increased humidity and high air temperature contributed to the intensive development of Alternaria sp. on tomato crops. P. infestans oomycete actively developed since the second half of August. The mass spreading of the pathogen was recorded in the second decade of September with a combination of optimal weather conditions: air humidity above 80 % at night, air temperature from + 20 °C to + 24 °C in the daytime.
The infestation area under the disease progression curve (AUDPC) was calculated for each genotype in each replication using an expanded modified formula [25]. Pearson correlation coefficients for various variables were calculated using the StatSoft Statistica V. 10.0 software package for statistical analysis.

Results and discussion
The first symptoms of Alternaria sp. in the form of dark spots were noted in the second decade of June. During the growing season, the disease developed in all aerial parts of plants. The intensity of Alternaria sp. development averaged 27.2 % ( Table 2).
The first signs of P. infestans infection appeared in the second decade of August. On average, the intensity of P. infestans development was 48.1 % during the growing season (  Significant correlation was noted (r = 0.98 at P <0.01). The relationship between the resistance of genotypes to diseases was average (r = 0.47-0.48 at P <0.05; r = 0.55-0.56 at P <0.05) ( Table 3).