Meloidogyne incognita (Kofoid & White) Chitwood, 1949
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.
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,
(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 Meloidogyninae, 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).
Vegetables, cereals, ornamentals, pasture, trees and shrubs, sugarcane, tobacco,
cotton, potatoes, etc.
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
Abnormal partitioning of photosynthates to the feeding site of the nematode.
Direct reduction of yield in many
Galled tomato roots
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
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
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
(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).
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
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.
Thomas SH, Schroeder J, Murray LW. 2004. Cyperus tubers protect
Meloidogyne incognita from 1,3-dichloropropene. J. Nematology 36: 131-136.