Cucurbit Genetics Cooperative Report 15:84-86 (article 33) 1992
B.B. Rhodes, Xingping Zhang, Ralph A. Dean, Jennifer Frick, and Jian Nong Zhang
Department of Horticulture, E-142 Poole Agricultural Center, Clemson University, Clemson, SC 29634-0375, Department of Plant Pathology and Physiology, B-03 Long Hall, Clemson University, Clemson, SC 29634, and Melon Research Institute, Gansu Agricultural University, Lanzhou, Gansu 730070 PRC
Love and Rhodes (2, 3) studied race 2 anthracnose resistance in populations from a diallel cross among the susceptible watermelon variety ‘New Hampshire Midget’ and three disease resistant sources: PI 299379, PI 189225 and a Citrullus colocynthis, ‘R309’. We concluded that resistance in both PI 299379 and PI 189225 was governed by a single dominant gene with modifiers. Suvanprakorn and Norton (4) had resported a dominant gene in PI 189225, PI 271778 and PI 326515. Resistance in ‘R309’ appeared to be controlled by several dominant genes different from the one in the 4 PI’s. Our studies were based on observations of whole plants in the field. This study was undertaken with detached leaves from the remainder of the populations generated in the previous study.
Fifty seed or less from families from the original study were planted in flats of soilless medium and watered daily. ‘Edisto’ muskmelon and ‘Butternut’ squash were also used to differentiate races. The second or third true leaf was detached in inoculated with drops of a 106 spore suspensions of anthracnose isolates in order to evaluate isolates. Finally, a single isolate of race 1 and race 2 was replicated by drops on each detached leaf, and lesion size was recorded with a micrometer five days after inoculation. Leaves were kept moist and exposed to fluorescent light in a transparent polyethylene chamber lined with filter paper. Six-week-old seedlings were transplanted into a 15-year monoculture area at the Edisto REC at Blackville. Surviving plants were considered resistant to wilt. thus, each individual from a specific family was rated for anthracnose lesion size using race 1 and race 2 isolates and survival in the presence of Fusarium wilt. Fusarium wilt resistance will be discussed separately.
Results of inoculations with race 1 and race 2 are given in Table 1 in terms of leaves with and without lesions, lesion size and the associated sample standard deviation.
The most obvious result from these inoculations is that escapes occurred. ‘New Hampshire Midget’ is susceptible to both races of anthracnose. Yet, 27% and 55% of the A plants were scored resistant to race 1 and race 2, respectively. Escapes and the small populations limit analysis of the data. The reaction of the race 2 susceptible ‘Edisto’ melon check to our race 2 indicated resistance instead of susceptibility.
Inheritance of race 1 resistance
Incomplete dominance for race 1 is indicated in parents B and C to both races in the F1 hybrids with A. Both F1 populations have larger numbers of resistant individuals. Backcrosses to the resistant parent result in a larger number of resistant individuals. The F2 populations also have more resistant individuals. Dominance for resistance in B and C is indicated in the F1 hybrids with D. For race 1, backcross populations (B x D)B, B (B x D), C (D x C) and (D x C)C all suggest dominance for resistance in B and C. the best evidence that B and C are homozygous for the same dominant gene is the virtual absence of susceptible progeny in all the populations from the B x C and C x B crosses.
Backcrosses involving parent A to the resistant parent B or C indicate that one or more susceptible classes are being generated in the presence of the dominant gene. Susceptibility in the presence of the dominant gene is coming from the susceptible parent A because all the progeny of the cross B x C are resistant in contrast to the A x B and A x C progeny. Henderson, et al., (1) has shown that resistance level to anthracnose is affected by gene dosage. F2 populations of A x B and A x C classes fit 3:1 resistant:susceptible ratios for race 1.
F2 progeny from the A x D cross suggest that D may have a recessive gene for resistance to race 1; but, because escapes are evident in the parents, it is possible that all resistant progeny are escapes.
Inheritance of race 2 resistance
Because escapes are evident in the susceptible parent A, it is likely that escapes occurred in the progeny. Dominance is indicated in the F1 of the cross A x B. Backcrosses to B exhibit more susceptible progeny than backcrosses to A, but the F2 progeny from the cross A x B fit a 3:1 R:S ratio.
Segregation of all the progeny from the A x C cross suggests a single dominant gene for resistance. The backcrosses to parent A fit a 1:1 R:S ratio, and most of the progeny from the backcross to parent C are resistant. the F2 progeny also fit a 3:1 ratio.
Virtually all the progeny from the cross B x C are resistant to race 2 as expected from a cross between two homozygous parents. Resistance to race 2 parallels that of resistance to race 1. Similarly, dominance for resistance is indicated in parents B and C when crossed to parent D.
Relationships between resistance and susceptibility and race 1 and race 2 resistance
An attractive hypothesis to explain the presence of the susceptible class in the backcrosses to the resistant parent is a loose linkage between the dominant gene for resistance and another gene which allows the expression of resistance. When the resistant parent is crossed with parent A, crossing over may occur between the dominant gene for resistance and the modifier gene, resulting in two new recombinant gametes that contribute susceptible genes. The large number of individuals susceptible to both races in the backcrosses B (A x B) and (A x B)B support this hypothesis.
In this small data set, the presence and size of a race 1 lesion was positively correlated with the presence and size of a race 2 lesion in all the lanatus families. Thus, in crosses with two known race 2 resistant lines, segregation for race 2 resistance paralleled segregation for race 1 resistance.
Table 1. Number of individuals with (S) or without (R) anthracnose lesions on detached leaves from Citrullus lanatus, Citrullus colocynthis, Cucumis melo and Cucurbita moschata drop inoculated with race 1 and race 2 isolates and maintained in a moist, illuminated polycarbonate chamber.
Observed: Race 1 |
Lesion Sizez |
Sample SDy |
Observed: Race 2 |
Lesion Sizez |
Sample SDy |
|
Parents and Checks |
R:Sw |
R:Sw |
||||
| New Hampshire Midget (A) | 3:8 | 1.46 | 0.79 | 6:5 | 0.48 | 0.15 |
| PI 299379 (B) | 20:0 | 0 | 0 | 19:1 | 0.50 | 0 |
| PI 189225 (C) | 15:1 | 2.60 | 0 | 15:1 | 3.20 | 0 |
| C. colocynthis ‘R309’ (D) | 1:5 | 1.02 | 0.96 | 2:4 | 0.90 | 0.73 |
| ‘Edisto’ muskmelon | 1:8 | 0.57 | 0.39 | 9:0 | 0 | 0 |
| ‘Butternut’ squash | 5:0 | 0 | 0 | 5:0 | 0 | 0 |
| Progeny | ||||||
| AxB | 7:3 | 0.70 | 1.04 | 8:2 | 1.10 | 1.13 |
| A(AxB) | 5:7 | 1.29 | 0.94 | 10:1 | 0.40 | 0 |
| (AxB)A | 13:13 | 1.22 | 1.07 | 21:5 | 1.40 | 0.99 |
| B(AxB) | 22:14 | 1.42 | 0.79 | 19:17 | 2.28 | 1.27 |
| (AxB)B | 40:27 | 1.15 | 1.38 | 55:12 | 0.60 | 0.42 |
| (AxB)F2 | 34:26 | 0.54 | 0.48 | 44:16 | 0.43 | 0.29 |
| AxC | 11:5 | 0.55 | 0.25 | 13:3 | 0.40 | 0.08 |
| A(AxC) | 11:6 | 1,58 | 0.68 | 9:8 | 1.98 | 1.25 |
| (AxC)A | 20:16 | 2.70 | 1.18 | 12:13 | 1.70 | 1.05 |
| (AxC)C | 29:6 | 3.52 | 1.39 | 33:2 | 1.55 | 1.06 |
| (AxC)F2 | 22:11 | 1.50 | 1.57 | 28:5 | 2.40 | 1.76 |
| AxD | 6:7 | 1:57 | 1.04 | 10:3 | 0.40 | 0.14 |
| (AxD)A | 1:0 | 0 | 0 | 1:0 | 0 | 0 |
| (AxD)F2 | 5:37 | 2.19 | 0.90 | 24:18 | 1.34 | 0.62 |
| BxC | 16:0 | 0 | 0 | 14:2 | 1.05 | 0.64 |
| CxB | 10:1 | 0 | 0 | 10:0 | 0 | 0 |
| (BxC)B | 30:2 | 1.80 | 2.12 | 32:0 | 0 | 0 |
| (BxC)C | 32:0 | 0 | 0 | 32.0 | 0 | 0 |
| C(BxC) | 39:1 | 0.90 | 0 | 38.2 | 0.50 | 0.28 |
| (BxC)F2 | 30:1 | 0.5 | 0 | 31.0 | 0 | 0 |
| DxB | 8:6 | 1.85 | 2.41 | 12:2 | 2.80 | 3.39 |
| D(DxB) | 2:2 | 1.60 | 1.84 | 4:0 | 0 | 0 |
| B(DxB) | 33:4 | 3.10 | 3.54 | 34:3 | 2.00 | 0 |
| (DxB)B | 15:1 | 0.40 | 0 | 14:2 | 1.00 | 0 |
| DxC | 16:0 | 0 | 0 | 16:0 | 0 | 0 |
| C(DxC) | 17:0 | 0 | 0 | 17:0 | 0 | 0 |
| (DxC)C | 33.2 | 1.15 | 0.21 | 35:0 | 0 | 0 |
| D(DxC) | 16.0 | 0 | 0 | 13:3 | 0.35 | 0.07 |
| (DxC)D | 6:0 | 0 | 0 | 2:4 | 0.88 | 0.76 |
z Lesion size in millimeters.
y Sample standard deviation, using n-1 weighting.
w Plants with leaves with lesions after inoculation were classified as “susceptible”, and the mean lesion size of susceptible plants and the associated SSD are recorded here.
Literature Cited
- Henderson, W.R. and S.F. Jenkins, Jr. 1977. Resistance to anthracnose in diploid and polyploid watermelons. J. Amer. Soc. Hort. Sci. 102(6):693-695.
- Love, S.L. and B.B. Rhodes. 1988. Single gene control of anthracnose resistance in Citgrullus ? Cucurbit Genetics Coop. Rpt. 12:5-6.
- Love, S.L. and B.B. Rhodes. 1991. R309, a selection of Citrullus colocynthis with multigenic resistance to Colletotrichum lagenarium race 2. Cucurbit Genetics Coop. Rpt. 14:92-96.
- Suvanprakorn, K. and J.D. Norton. 1980. Inheritance of resistance to race 2 anthracnose in watermelon. J. Amer. Soc. Hort. Sci. 105:862-865.