These Dominant genes confer the ability to resist the negative effects of different diseases.
They are introgressions, genes found in wild relatives, that were discovered and bred into tomatoes by people like Charles Rick and his colleagues at the TGRC.
They act by recognizing the pathogen and initiating an immune response, often involving a hypersensitive reaction (localized cell death) that stops the pathogen from spreading, in effect “cutting it off.”
Cf-1 Leaf mold (Cladosporium fulvum) from Solanum pimpinellifolium (1937)
Cf-2 Leaf mold (Cladosporium fulvum) from Solanum pimpinellifolium or S. pennellii
Cf-3 Leaf mold (Cladosporium fulvum) from Solanum pimpinellifolium or S. habrochaites
Cf-4 Leaf mold (Cladosporium fulvum) from Solanum hirsutum
Cf-ECp5 Leaf mold (Cladosporium fulvum) from Solanum pimpinellifolium
ETC
Tm-1 Tobacco Mosaic Virus resistance; from Solanum pennellii
Interacts with ToMV replication proteins, preventing the virus from forming a replication complex with host membranes. Tm-1 combined with a specific tolerance locus on chromosome 11 is essential for effective resistance
Tm-2 Tobacco Mosaic Virus resistance and and Tomato Mosaic Virus resistance, but not Tomato Brown Rugose Fruit Virus (ToBRFV); from Solanum peruvianum
Currently, the industry is focusing on developing new resistance mechanisms, such as the HREZ (High Resistance) technology from Enza Zaden, to protect tomato crops from Tomato Brown Rugose Fruit Virus (ToBRFV). Functions in a similar, robust manner to the industry-standard Tm-2-2, and is related.
Mi- Nematode resistance (Meloidogyne incognita and two other species); from Solanum pervianum (1940s)
,NBS-LRR (nucleotide-binding, leucine-rich repeat) resistance gene that confers immunity against root-knot nematodes and certain sap-sucking insects. It triggers a localized hypersensitive response (cell death) at the infection site to restrict pest feeding, but this defense fails in soil temperatures above 28C
I-3 gene Fusarium vascular wilt (Fusarium oxysporum race 3); from Solanum pennellii. It encodes a S-receptor-like kinase (SRLK) that recognizes the fungus
I-2 and I-1 genes Fusarium vascular wilt (Fusarium oxysporum race 2 and 1); from Solanum pimpinellifolium
Ph-1 Late blight (Phytophthora infestans oomycete); from Solanum pimpinellifolium
recognizes pathogen and triggers a localized, hypersensitive cell death response to halt infection. One of the first resistance genes introduced into commercial tomato cultivars. While Ph-1 is largely ineffective on its own, it has been used in conjunction with other resistance genes, such as Ph-2 and Ph-3, to develop more robust, stacked resistance in modern breeding
Ph-2 Late blight (Phytophthora infestans oomycete); from Solanum pimpinellifolium
CC-NBS-LRR disease-resistance protein that triggers a hypersensitive response (localized cell death) to combat the pathogen. Provides resistance against a wide range of P. infestans races, though it is considered partial resistance rather than immunity.
Ph-3 Late blight (Phytophthora infestans oomycete); from Solanum pimpinellifolium
CC-NBS-LRR disease-resistance protein that triggers a hypersensitive response (localized cell death) to combat the pathogen. Provides resistance against a wide range of P. infestans races, considered the strongest of the three.
Ve- Verticilium wilt (Verticillium dahliae and V. albo-atrum,); ancient origin
encodes cell-surface glycoprotein receptors on the plasma membrane, which recognize fungal effectors and initiate an immune response;
