Rev 07/03/2024
Tylenchida Tylenchina Tylenchoidea Meloidogynidae Meloidogyninae
Meloidogyne incognita (Kofoid & White, 1919) Chitwood, 1949
Review general characteristics of the genus Meloidogyne.
Reported median body size for this species (Length mm; width micrometers; weight micrograms) - Click:
Major significance in tropics and warmer regions.
C-rated pests in California.
Sedentary endoparasite.
Feeding site establishment and development typical of genus.
Since nematodes in the Heteroderidae become sedentary from the late second stage onwards (except for the metamorphosis to males), the feeding site in the plant must be maintained in a condition favorable for perhaps five or six weeks to allow the nematode to fulfill its reproductive potential. Besides stimulation of the cell cycle events, pathogen-triggered immunity (PTI) responses, including activation of the salicylic acid pathway, must be suppressed. The salicylic acid pathway leads to production of active oxygen molecules and hypersensitive cell death. In the Meloidogynidae, a possible candidate for effector-triggered suppression of PTI is chorismate mutase, produced in the nematode esophageal glands. In PTI responses, chorismate is converted to salicylic acid to iniate the defense events. Chorismate mutase from the nematode reduces chorismate, and thus salicylic acid (Smant and Jones, 2011).
Type Host: Carrot (Daucus carota) via fecal samples.
Vegetables, cereals, ornamentals, pasture, trees and shrubs, sugarcane, tobacco, cotton, potatoes, etc.
Ecophysiological Parameters:
Chromosome number 2n=32-28 and 2n=41-46. The large number, and variability of chromosome number, are typical of species reproducing by obligate mitotic parthenogenesis. (Eisenback and Triantaphyllou, 1991; ; Subbotin et al., 2021; Triantaphyllou, 1985).
Meloidogyne incognita is involved in many disease interactions, eg blackshank of tobacco (Phytophthora parasitica var nicotianae), Granville wilt (Pseudomonas solanacearum) - resistant plants predisposed by M. incognita. Field trials with combined inoculations reduced tobacco crop values by $800/acre over the nematode alone. Resistance to M. incognita has been a very important solution to these complexes.
The tobacco industry in some counties of NC was saved by incorporating M. incognita resistance into the genome (NC95 the resistant variety). These interactions are especially important because of the research effort and consequent understanding. N.T. Powell was a pioneer in this area. He also showed that plants infected 4 weeks previously by M. incognita were susceptible to infection and decay by Pythium and Rhizoctonia, which are usually only important in seedling diseases.
Powell also showed that "non-pathogens" of tobacco, including Curvularia, Botrytis, Aspergillus, Penicillium and even Trichoderma can invade the altered root system and cause extensive decay.
The biopredisposition is thought to be more through physiological rather than mechanical effects.
The cotton cultivar Acala SJ2 is predisposed to Fusarium wilt by M. incognita, requiring nematode control where both pathogens occur in the southern San Joaquin valley of California. Acala SJ5 is tolerant to Verticillium wilt, but that cultivar is also predisposed by M. incognita.
Disruption of the vascular system.
Abnormal partitioning of photosynthates to the feeding site of the nematode.
Direct reduction of yield in many crops.
Galled tomato roots
Nematicides:
Nematicides have been very important. They may, however, be less effective when nematodes are embedded in plant tissue. For example, tuber viability of yellow nutsedge (Cyperus esculentus) and purple nutsedge (Cyperus rotundus), and survival of M. incognita harbored within them were unaffected by 1,3-D treatment (Thomas et al, 2004).
Host Plant Resistance, Non-hosts and Crop Rotation alternatives:
Sources of host-plant resistance to M. incognita occur in several plant genera, including clovers, cotton, peach (e.g. Nemaguard), peanut, pineapple, corn, sweetpotato, tobacco and tomatoes.
Use of tobacco cultivars resistant to M. incognita in North Carolina, based on the resistance gene first introduced into cultivar NC95, has resulted in selection for the more virulent (to tobacco) M. arenaria and M. javanica..
The Mi gene of tomato is a single dominant gene that confers resistance to M. incognita, M. javanica, and M. arenaria. It is located near the centromere of chromosome 6. Bailey (1940) provided an early report of the wild tomato species Solanum peruvianum as a source of resistance to root-knot nematodes. Due to reproductive incompatibilities between the Solanum lycopersicum and S. peruvianum, embryos resulting from crosses do not reach maturity. Consequently, techniques for embryo rescue techniques were developed in which immature embryos are dissected from seed and cultured axenically. The technique appears to have been first used to transfer the Mi gene from wild tomato into commercial cultivars by Smith (1944) in crossing Solanum lycopersicum var. Michigan State with S. peruvianum PI128.657.
Dr. Charles Rick and colleagues at UC Davis discovered that an isozyme, acid phosphatase, is coded by the gene Aps-1 which is located on chromosome 6 of tomato close to, and tightly linked with, Mi (Rick and Fobes, 1974). The isozyme provides a tool for tomato breeders to determine whether they have successfully transferred Mi into commercial varieties and has facilitated the development of processing varieties with root-knot nematode resistance.
The Mi gene has been cloned and sequenced in the laboratory of Dr. Valerie Williamson at UC Davis. Using Agrobacterium as a carrier, the resistance gene has been transferred to a susceptible tomato cultivar, which expresses the resistance. Plants grown from seeds of the transgenic plant are also resistant to M. incognita. However, after the second generation of plant offspring, the expression of resistance is progressively reduced in seed batches from some plants but not from others. In both cases, the gene is still present and is still coding for RNA (Goggin et al, 2004).
The resistance conferred by the Mi gene breaks down at soil temperatures >28C.
The expression of resistance by the Mi gene is cell death, the death of the nematode feeding site. This is often referred to as the hypersensitive response. The reaction is essentially an effector-triggered immunity, although the nature of the effector is unknown at this time.
With repeated use of the single source of resistance in California tomato production, aggressive strains of the nematode are being selected (Kaloshian et al. 1996).
In the early 1990s, farm advisors and entomologist Dr. Harry Lange noticed that tomatoes with the Mi gene appeared to be also resistant to the potato aphid, Macrosiphum euphorbiae. Initial determination was that a gene tightly linked to Mi and designated Meu1 was responsible for the potato aphid resistance. Current research indicates, however, that the two genes are identical and that Mi confers resistance to both root-knot nematodes and the potato aphid. A more recent development is the discovery that the Mi gene also confers resistance against the white fly Bemisia tabaci (Nombela et al., 2003). The gene is located near the centromere of tomato chromosome #6.
As with the resistance to M. incognita, the resistance to the potato aphid is also progressively reduced after the the second generation of plant progeny (Goggin et al, 2004).
Cultural Management:
Minimizing post-harvest reproduction:
Bailey, D.M. 1940. The seedling test method for root-knot nematode resistance. Proc. Amer. Soc Hort. Sci. 38:573-575.
CIH Descriptions of Plant-parasitic Nematodes, Set 2, No. 18 (1973).
Goggin FL, Shah G, Williamson VM, Ullman DE. 2004. Instability of Mi-mediated nematode resistance in transgenic tomato plants. Molecular Breeding 13:357-364.
Eisenback, J.D. and Triantaphyllou, H.H. 1991. Root-knot nematodes: Meloidogyne specues and races. In W.R. Nickle (ed) Manual of Agricultural Nematology. Marcel Decker, New York, USA
Kaloshian, I., V.M. Williamson, G. Miyao, D.A. Lawn and B.B. Westerdahl. 1996. "Resistance-breaking" nematodes identified in California tomatoes. California Agriculture 50(6):18-19.
Lu, P., Davis, R.F., Kemerait, R.C. (2010). Effect of mowing cotton stalks and preventing plant re-growth on post-harvest reproduction of Meloidogyne incognita. Journal of Nematology 42:96-100.
Nombela, G., V. M. Williamson, and M. Muniz. 2003. The root-knot nematode resistance gene Mi-1.2 of tomato is responsible for resistance against the whitefly Bemisia tabaci. Mol. Plant Microbe Int. 16:645-649.
Rick, C.M. and Fobes, J.F. 1974. Association of an allozyme with nematode resistance. Rep. Tomato Genet. Coop 24:25.
Smith, P.G. 1944. Embryo culture of a tomato species hybrid. Proc. Amer. Soc Hort. Sci. 44:413-416.
Subbotin, S.A. Palomares-Rius, J.E., Castillo, P. 2021. Systematics of Root-knot Nematodes (Nematoda: Meloidogynidae). Nematology Monographs and Perspectives Vol 14: D.J. Hunt and R.N. Perry (eds) Brill, Leiden, The Netherlands 857p.
Thomas SH, Schroeder J, Murray LW. 2004. Cyperus tubers protect Meloidogyne incognita from 1,3-dichloropropene. J. Nematology 36: 131-136.
Triantaphyllou, A.C. 1985. Gametogenesis and the chromosomes of Meloidogune nataliei: not typical of other root-knot nematodes. J. Nematology 17:1-5.
Triantaphyllou, A.C. 1985. Cytogenetics, cytotaxonomy and phylogeny of root-knot nematodes. In Sasser, J.N. & Carter, C.C. (eds) An Advanced Treatiswe on Meloidogyne.Vol 1. Biology and Control.N.C. State Universty Graphics, Raleigh, N.C. USA.