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Review
. 2019 Nov 14;10(11):925.
doi: 10.3390/genes10110925.

Tomato Natural Resistance Genes in Controlling the Root-Knot Nematode

Ahmed H El-Sappah  1   2   3 , Islam M M  1   2 , Hamada H El-Awady  1   2 , Shi Yan  1   2 , Shiming Qi  1   2 , Jingyi Liu  1   2 , Guo-Ting Cheng  1   2 , Yan Liang  1   2
Affiliations
Review

Tomato Natural Resistance Genes in Controlling the Root-Knot Nematode

Ahmed H El-Sappah et al. Genes (Basel). .

Abstract

The root-knot nematode (RKN) is one of the most dangerous and widespread types of nematodes affecting tomatoes. There are few methods for controlling nematodes in tomatoes. Nature resistance genes (R-genes) are important in conferring resistance against nematodes. These genes that confer resistance to the RKN have already been identified as Mi-1, Mi-2, Mi-3, Mi-4, Mi-5, Mi-6, Mi-7, Mi-8, Mi-9, and Mi-HT. Only five of these genes have been mapped. The major problem is that their resistance breaks down at high temperatures. Some of these genes still work at high temperatures. In this paper, the mechanism and characteristics of these natural resistance genes are summarized. Other difficulties in using these genes in the resistance and how to improve them are also mentioned.

Keywords: Mi resistance genes; gene-based marker; heat-stable resistance; root-knot nematode; tomato-resistant resources.

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Conflict of interest statement

The authors have no conflicts of interest to report.

Figures

Figure 1
Figure 1
Distribution of Meloidogyne species; three types of distribution: (1) black marks indicate present, (2) red marks indicate widespread, and (3) blue marks indicate restricted.
Figure 2
Figure 2
The mechanism of natural resistance against the root-knot nematode (RKN). (a) In susceptible plants, where there are no Mi-genes, the nematode completes its life cycle in the root by forming giant feeding cells. (b) In the resistance case, the plant undergoes the first defense line against RKN penetration by the interaction between extracellular receptor proteins, receptor-like kinases (RLK), receptor-like protein (RLP), and nematode effectors. (c) The plant then begins the second defense line, which includes direct gene-for-gene interaction. This theory depends on direct interaction between the receptor protein of tomatoes and nematode effectors, producing Mi-proteins, which prevent the nematode from feeding. No giant cell formation is observed. (d) The other second defense line is an indirect pathway, which is referred to as the guard hypothesis. In these cases, the virulence factor of the nematode (Avr genes) interacts with tomato accessory protein.
Figure 3
Figure 3
Hypersensitive response of Mi-1 after nematode infection. The nematode Avr genes trigger the tomato Mi-1 resistance gene(R-gene) to be active under the salicylic acid pathway with inhibition by both cytokinin and high temperature.
Figure 4
Figure 4
Mapping of Mi genes on tomato chromosomes; (a) the site of Mi-1, Mi-9, and Mi-HT on chromosome 6; (b) the site of Mi-3 and Mi-5 on chromosome 12.
Figure 5
Figure 5
The effect of temperature on both resistant plants and nematodes. A temperature from 18 to 28 °C is suitable for both plants and nematodes. With a temperature up to 28 °C, the Mi-1 gene in resistant plants becomes inactive, and at the same time, the nematode becomes more dangerous. The nematode activity decreases when the temperature exceeds 32 °C.
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