Watermelon
Crop Information
Disease, Insect, and Stress Resistance
- by Todd C. Wehner
- Department of Horticultural Science
- North Carolina State University
- Raleigh, NC 27695-7609
Disease
Seedling Tests. Disease resistance is
an important objective of most breeding programs. Screening
for resistance to several important diseases using greenhouse
seedling tests is useful, and provides several advantages.
Plants that are found to be resistant to the diseases being
tested can be transplanted from the test flats to soil or
other growth medium in bags or pots where they can be grown
and self-pollinated, or crossed with other lines. Greenhouse
tests can be run at a time when plants cannot be grown outside,
permitting more generations of testing each year, and the
disease testing greenhouses can be isolated from other watermelon
research to keep the diseases from spreading. At North Carolina
State University, gummy stem blight tests are isolated in
one area, and virus tests in another area so that the diseases
do not spread to a third area where the other breeding work
is located.
For some diseases such as anthracnose, it is useful to
have a humidity chamber to incubate the disease after inoculation.
A humidity chamber can be built on a greenhouse bench using
one humidifier for each 24 sq. ft. of bench area. An air
conditioner can be used to keep the temperature cool, since
some diseases do best in cool and humid conditions. The
greenhouse temperature is usually kept between 75° and
95°F for optimum plant growth, and the humidity chamber
is usually kept between 65° and 75°F for optimum
disease development. A less expensive option for disease
chambers is to build a frame on a greenhouse bench and cover
it with polyethylene film on the top and sides. Humidifiers
placed inside the chamber several hours before disease inoculation
should be able to raise the relative humidity above 95%.
Fusarium Wilt. Fusarium wilt is caused
by Fusarium oxysporum f. sp. niveum (see
Figs. 7.17-7.20). The disease was first reported in 1889
in Mississippi, and was widespread throughout the southern
parts of the United States by 1900. Three types of pathogen
spores are commonly observed: small, colorless, oval, non
septate microconidia; large, sickle shaped, septate macroconidia;
and thick walled circular chlamydospores. There are three
races known: 0, 1, and 2. Most current varieties are resistant
to race 0, and some also are resistant to race 1. Race 2
was discovered more recently, and occurs mainly in the south
central production areas such as Texas and Oklahoma, but
it also has been found in Florida.
Race 0 causes wilt in older, susceptible varieties such
as ‘Florida Giant’, ‘Black Diamond’,
and ‘Sugar Baby’. Race 1 is more virulent than
race 0 and affects more plants within susceptible varieties,
but does not affect resistant 'Calhoun Gray'. Race 2 is
highly virulent and can affect otherwise resistant varieties
such as 'Calhoun Gray', 'Summit', 'Smokylee', and 'Charleston
Gray'. Races of fusarium can be identified using differentials.
'Sugar Baby' and 'Black Diamond' are susceptible to all
the three races; 'Quetzali', 'Mickylee', 'Charleston Gray',
and ‘Crimson Sweet’ are susceptible to races
1 and 2, while 'Calhoun Gray' is susceptible to only race
2. Resistance to race 2 is available in PI 296341 and PI
271769.
- Fusarium wilt race
- 0 1 2 Variety or accession
- S S S Black Diamond (or Sugar Baby)
- R S S Quetzali (or Mickylee)
- R M S Charleston Gray (or Crimson Sweet)
- R R S Calhoun Gray
- R R R PI 296341 (or PI 271769)
Fusarium can survive in soil as a saprophyte. The pathogen
is spread locally by moving soil, compost, manure, water,
tools, and machinery from one field to another, as well
as by humans and animals moving between fields. The pathogen
can also persist on infested seeds for more than 2 years.
Fusarium enters plants through root tips and openings in
roots where lateral roots emerge. Presence of root-knot
nematodes is also thought to increase the incidence of the
disease. After penetration, the fungus grows into the xylem
where it accumulates materials that plug the xylem and cause
wilting. Watermelon is attacked at all growth stages by
the pathogen. At the seedling stage there is damping-off,
and cotyledon wilt results in slower growth and stunting.
The vascular tissue inside wilted stems may be discolored.
A white or pink colored fungus growth usually appears on
the surface of dead stems in wet weather conditions. The
ideal temperature for infection and disease development
is 80°F. However, seedling rot occurs at soil temperatures
of 61º to 65°F, while seedling wilt is severe between
77º to 82°F. The disease is also promoted by high soil
organic matter.
The first fusarium wilt resistant variety ‘Conqueror’
was released in 1908. It was developed by W.A. Orton of
the USDA using a wilt-resistant citron accession crossed
with 'Eden'. 'Conqueror' did not have high fruit quality,
so was not grown much after its release. However, varieties
developed using resistance from 'Conqueror' such as 'Iowa
Belle' and 'Iowa King' had improved fruit quality, so were
used commercially. More recent varieties such as ‘Calhoun
Gray’, ‘Smokylee’, and ‘Dixielee’
have resistance, as well as improved horticultural performance.
Two types of fusarium wilt resistance are known, having
different patterns of inheritance. Resistance to race 1
in 'Calhoun Gray' is controlled by a single dominant gene,
with some modifier genes, and provides a high level of resistance
that is easy to transfer into new breeding lines. There
is also a source of resistance to race 1 which is controlled
by several recessive genes. That source of resistance has
been difficult to fix at a high level in stable, inbred
lines. Varieties resistant at high inoculum levels are 'Dixielee'
and 'Smokylee'. In wild species, resistance to fusarium
has been reported to be polygenic. Resistance to race 2
has been reported in PI 296341, and the selection PI 296341-FR
is resistant to all three races of fusarium. Also, PI 271769
was reported to be highly resistant to race 2.
Anthracnose. Anthracnose caused by Colletotrichum
lagenarium is an important disease of watermelon in
the United States (see Figs. 7.3-7.6). Symptoms caused by
this pathogen may occur on leaves, stems, and fruit. Lesions
on leaves are irregular shaped, limited by the leaf vein,
and brown to black in color. Lesions on the stem are oval
shaped and tan colored with a brown margin. Lesions similar
to those found on stems and leaves also appear on the fruit.
Older fruit show small water-soaked lesions with greasy,
yellowish centers that are somewhat elevated.
Seven races of the anthracnose pathogen have been reported.
Races 4, 5, and 6 are virulent in watermelon, but races
1 and 3 are most important. Many varieties are resistant
to races 1 and 3, and resistance to race 2 will be needed
in the near future.
The first source of resistance to anthracnose was identified
in an accession, Africa 8, sent to D.V. Layton of the USDA
by R.F. Wagner in Umtali, South Africa. Layton developed
anthracnose resistant 'Congo', 'Fairfax', and 'Charleston
Gray' from that source. Resistance was later found to be
inherited as a single dominant gene, Ar-1. The gene provides
resistance to races 1 and 3, but not to race 2. 'Crimson
Sweet' and many other current varieties have that source
of resistance. Several genes were found to be responsible
for resistance to Race 2.
PI 189225, PI 271775, PI 299379, and PI 271778 have been
reported to carry resistance to complex Colletotrichum species.
Some of the other sources of resistance to anthracnose reported
in the literature are PI 203551, PI 270550, PI 326515, PI
271775, PI 271779, and PI 203551. 'R 143' was reported to
be resistant to race 2 of the pathogen. PI 512385 had the
highest resistance to race 2 of the pathogen from a screening
test involving 76 plant introductions.
Gummy Stem Blight. Watermelon is one of
the most susceptible of the cucurbit species to gummy stem
blight, caused by Didymella bryoniae (see Figs. 7.21-7.25).
The disease occurs throughout the southern United States,
particularly the southeast. Field and greenhouse tests are
available, but the results are variable, and it can be difficult
to get reproducible results.
The USDA collection of plant introduction accessions has
been screened for gummy stem blight resistance by several
teams of researchers. Some accessions have resistance to
the disease, including PI 189225 and PI 271778.
Powdery Mildew. Watermelon is one of the
most resistant cucurbit species to powdery mildew (Sphaerotheca
fuliginea) (see Figs. 7.28-7.30). However, there are a few
regions of the world where powdery mildew is a problem on
watermelon. For example, watermelons grown in southern India
are affected with the disease, but not in northern India.
In southern India, 'Arka Manik' is resistant to powdery
mildew. The pm gene causes susceptibility to the disease,
but most varieties have the resistance allele. Powdery mildew
is becoming more of a problem in the United States, especially
in the western states, and has been reported in the southeastern
states as well.
Yellow Vine. Yellow vine is a relatively
new disease of watermelon, caused by an unknown, phloem-limited
bacterium. Evidence indicates that leafhoppers vector the
disease. The disease was first observed in central Texas
and Oklahoma in 1991 and has caused severe losses in early-planted
watermelon in some years. In 1998, the disease was detected
in watermelon and pumpkin in Tennessee. Production areas
of Georgia, Florida, and other parts of southeastern United
States may be at risk in the future. Low levels of resistance
or tolerance have been identified in a few open-pollinated
and hybrid varieties, although the mechanism of resistance
is unknown. Research is needed to identify good sources
of resistance.
Bacterial Fruit Blotch. Bacterial fruit
blotch of watermelon is a serious disease of seedlings and
fruit caused by Acidovorax avenae subsp. citrulli (see Figs.
7.8-7.13). Disease incidence increases under high humidity
or where overhead irrigation is used. The disease was first
reported to occur in commercial watermelon production areas
in the United States in 1989. Early-season outbreaks can
result in total loss of fruit by harvest time. Bacterial
fruit blotch is also reported to attack cantaloupe fruit
in the field, as well as other cucurbits. Bacterial fruit
blotch epidemics during 1994 in certain states in the United
States resulted in litigation, and had a devastating effect
on the watermelon industry. Currently, most seed companies
require growers to sign waiver forms to reduce the possibility
of litigation. Some companies have restricted seed sales
in certain states where the risk of disease is high. Seed
costs have increased due to the changes in the seed handling,
packaging and testing required for reducing the incidence
of disease.
The characteristic symptoms of bacterial fruit blotch are
the appearance of a dark olive green stain, or blotch, on
the upper surface of infected fruit. Apart from attacking
the fruit, the pathogen is also reported to attack the leaves
and seedlings, and can be seed transmitted. D.L. Hopkins
and co-workers reported that fermentation of seeds for 24
to 48 hours followed by 1% hydrochloric acid or 1% calcium
hypochlorite treatment for 15 minutes prior to washing and
drying were the most effective treatments for bacterial
contaminated watermelon seeds. This treatment is for diploids;
triploid seed germination is drastically reduced by fermentation.
However, an effective, cost efficient, and environmentally
safe method for disease control would be development of
resistant varieties.
A seedling test for early screening of watermelon fruit
blotch was developed in 1992, and research on a few watermelon
lines using this test has been reported. There has been
some research to identify genetic resistance in the watermelon
germplasm collection. Based on seedling tests, PI 295843
and PI 299378 were reported to be resistant to the pathogen.
In 1993, D.L. Hopkins and co-workers conducted a study of
22 varieties and 2 PI accessions for resistance to fruit
blotch of watermelon and reported that none were immune
to the pathogen. Research is underway to find sources of
resistance in the germplasm collection.
Fruit resistance to the pathogen appears to be related
to rind color and ploidy, with diploid varieties having
light rind color being most susceptible and triploid varieties
with dark rind color being less susceptible. Fruit with
stripes appeared to be intermediate in their resistance.
Detached leaf tests have been developed that are effective
in screening plants for resistance in a breeding program.
Bacterial Rind Necrosis. Bacterial rind necrosis is caused
by Erwinia species. However, some other bacterial species
(Pseudomonas, Enterobacter, and Bacillus) are also known
to cause similar symptoms. Typical symptoms of bacterial
rind necrosis on watermelon fruit are characterized by a
light brown, dry, hard area of discoloration interspersed
with light areas generally limited to the rind (see Fig
7.7). The disease was first reported in Texas in 1968. The
most resistant varieties in studies conducted in Florida
over a 3-year period were 'Sweet Princess' and 'Jubilee',
while the most susceptible were 'Klondike Blue Ribbon' and
'Louisiana Queen'.
Root-knot Nematodes. Watermelon is susceptible
to root-knot nematodes caused by Meloidogyne spp. (see Figs.
6.1-6.3). The USDA collection of plant introduction accessions
is being screened for resistance. Root-knot resistance may
be an important future breeding objective if resistant accessions
are identified.
Virus Diseases. The main virus problems
in watermelon production in the United States are papaya
ringspot virus-watermelon strain (PRSV-W, formerly watermelon
mosaic virus-1), watermelon mosaic virus-2 (WMV-2) (see
Figs. 7.32-7.33), and zucchini yellow mosaic virus (ZYMV).
The watermelon germplasm collection has been screened for
resistance to some virus diseases. Accessions reported to
be resistant to WMV-2 are PI 244018 and PI 244019. Resistance
to ZYMV is found in PI 482299, PI 482261, PI 595203, and
PI 255137. Research is in progress to identify sources of
resistance to PRSV-W as well. Multiple virus resistance
will be an important breeding objective for new cultivars
in a few years.
Other Diseases. Verticillium wilt is an
increasing problem in the western United States, but little
is known about sources of resistance. Resistance to alternaria
leaf spot (see Figs. 7.1-7.2) has been identified in varieties
such as ‘Sugar Baby’, ‘Fairfax’,
and ‘Calhoun Gray’.
Physiological Diseases. Many of the watermelon
fruit defects have a genetic component. Breeders should
select lines to be free of defects under conditions conducive
to the problem. Fruit defects include hollowheart (see Fig.
7.34), rind necrosis (see Fig. 7.7), blossom-end rot (see
Fig. 7.35), and cross stitch (see Fig. 7.38). Hollowheart
is a separation of the tissue within the endocarp caused
by rapid fruit growth and weak tissue. More research is
needed to identify sources of defect resistance, and environmental
conditions that help reduce their frequency.
Insect Resistance Traits
Little research has been done on insect resistance in watermelon.
This may be due to the fact that most insect pests can be
controlled with insecticides. The major insect and arachnid
(arthropod) pests of watermelon are aphids (see Figs. 8.1-8.3),
pickleworm, spider mite (see Figs. 8.14, 8.15), and spotted,
striped (see Figs. 8.12, 8.13), and banded cucumber beetles.
PI 299563 is resistant to melon aphid (Aphis gossypii).
'Congo' and 'Giza 1' were the most resistant of five accessions
evaluated for resistance to spider mite. Several genes were
found to control non-preference type resistance to spotted
cucumber beetle in 'Hawkesbury' x a resistant accession.
Resistance to spotted and banded cucumber beetles was due
a single recessive gene.
A single dominant gene, Fwr, was responsible for resistance
to the melon fruit fly (Dacus cucurbitae) in the
watermelon line JI8-1. ‘Afghan’ is reported
to have resistance to red pumpkin beetle (Aulacophora
foveicollis), and 'Blue Ribbon' and 'Crimson Sweet'
are resistant to pickleworm.
Stress
Little research has been done on stress resistance in watermelon.
Water stress is an important cause of reduced yield in watermelon.
It may be that some genotypes are more efficient in water
use than others, but it probably will be difficult to develop
highly efficient varieties since watermelon fruit have very
high water content. In Israel, deep-rooted varieties are
used in unirrigated desert areas.
Pollination problems are responsible for improper fruit
development. It is necessary for all three lobes of the
stigma to be fully pollinated if the fruit is to develop
fully, and without curvature. Proper fruit development requires
adequate numbers of honeybees or bumblebees during flowering,
along with weather that is conducive to pollination. Bumblebees
can be more effective pollinators than honeybees. Cold,
rainy weather leads to poor pollen shed, and hot weather
often leads to reduced bee activity. In the case of triploid
hybrids, it is necessary to have up to one third of the
field planted to a diploid pollenizer to assure adequate
fruit development in the triploids which are male sterile.
Growers plant early in the season, often using transplants
and plastic mulch (with row covers in some cases) when there
is a danger of frost. Cucurbits are susceptible to chilling
injury at air temperatures below 42°F. Chilling injury
is a concern in watermelon because of the value of early
harvested fruit. There might be chilling resistance in the
watermelon germplasm collection that could be incorporated
into new varieties as has been done in other cucurbits.
Watermelon appears to be more chilling resistant than melon
and cucumber. Symptoms of chilling are white areas on the
cotyledons and white or light brown margins on the fully
expanded leaves. Chilling injury is increased by a longer
duration of chilling, lower temperature, high intensity
of light during chilling, high wind speed during chilling,
or a higher growth temperature before chilling occurs. Watermelon
is thermophilic, meaning that plants have a high optimum
growth temperature. Although the optimum is probably 80-90°F,
temperatures above 90°F reduce growth rate, and can
reduce fruit yield. Above 105°F, plants can be injured,
and young leaves will be light green with yellow margins.
Measles is a condition where green-brown spots develop
on the fruit surface, covering a small area or even the
entire surface, and starting out as minute watersoaked areas.
The spots become tan, slightly raised areas with necrotic
centers. The symptoms occur when excessive guttation is
encouraged by periods of high humidity or during the early
fall production season when the humidity is high and the
nights are cool. The fruit symptoms become evident 21-25
days after the conducive environmental conditions occur.
There is usually no economic loss from the stress, and it
might be controlled by reducing the amount of irrigation
in the fall production season.
