Cucurbit Genetics Cooperative Report 16:47-48 (article 17) 1993
Henry M. Munger
Department of Plant Breeding, Cornell University, Ithica, NY 14853, USA
It is now 50 years since I saw melons near Geneva, N.Y. wilt and die just as the first fruits were ripening. This was in a field in which W.D. Enzie was breeding for improved horticultural features and was typical of what came to be called “sudden wilt”. Over the years since then, horticulturists and plant pathologists studyingthe problem in New York have implicated low soil temperatures, fusarium, pythium, and cucumber mosaic virus (CMV). However, the disorder has been so difficult to duplicate experimentally that there has been no consensus about the cause except that it is probably complex and can involve more than one agent.
In occasional years when sudden wilt is severe, differences have appeared in variety trials and breeding pots which offer some clues. The most frequent observation has been the superior survival of breeding lines and hybrids selected for cucumber mosaic resistance (CMR). On the other hand, there have so often failed to show superiority that other factors must have been more important or the level of the CMR has been inadequate.
One contributing factor may be powdery mildew. Over the past 30 years there have been three occasions when susceptible lines wilted while their PMR counteparts remained turgid. Even though mildew did not appear to be severs, temperature likewise reduces water uptake but by itself has not been shown to cause the wilting and death so often observed.
There have been two recent incidents in which viral resistance made a great difference in the survival of melons late in the season. In 1990, progenies segregating for WMV resistance (WMR), and with three backcrosses to Topmark, Honeydew, TAM Uvalde, and Cornell CPM339, were inoculated as seedlings with WMV and set in the field along with the susceptible recurrent parents. During pollination, the superiority of resistant segregates in all four backcrosses over the corresponding recurrent parents was evident, but it was also clear that CMV had come into the planting because CPM330, which has a moderate level of resistance, was the only recurrent parent to set fruit. Then in early September, as fruit was about half developed, the CPM330 plants collapsed and died, as did most of the WMR segregates except for those with backcrosses to CPM339. In short with both CMV and WMV present, resistance to either virus kept plants alive long enough to set fruit, and in most cases viable seed, but only those with resistance to both produced edible fruit.
In 1992, resistance to papaya ringspot virus (PRR) made a large difference in survival in a planting of diverse melons which we hoped would remain disease-free. One purpose was to compare fruit type of PR resistant Cornell PPM339 and its hybrids with its recurrent parent PM339 and its hybrids. PM339 has a low level of cucumber mosaic resistance and is also the recurrent parent of CPM339 mentioned above. Soon after transplanting, a few plants with virus symptoms were removed from the field, and PRV and CMV were both found to be present. Spread did not appear to be rapid through the flowering period, but plants began to die as fruit developed slowly in the cold wet season. In September the superior survival of PPM339 and its hyvrids as compared with their near-isogenic counterparts became evident and Table 1 gives the proportion of live plants just before frost.
Table 1. Proportion of live plants on September 22.
Row. No. |
Identity |
-PPR |
+PPR |
|
| 68, 69 | PM339 | 2/24 | ||
| 70,71 | PPM339 | 15/24 | ||
| 607 | PM339 X MR324 | 0/6 | ||
| 608 | PPM339 X MR325 | 3/6 | ||
| 615 | PM339 X TAM Uvalde | 1/6 | ||
| 616 | PM339 X TAM Uvalde | 2/6 | ||
| 638 | PM339 X Gulfcoast | 1/6 | ||
| 639 | PPM339 X Gulfcoast | 3/6 | ||
| Total | 4/42 | 23/42 |
It is doubtful that anyone would have suspected PRV as a cause of death had it not been for the isogenic comparisons. While we did not follow symptoms closely in this case, we have often seen in the past that when CMV infection occurs late in the season, there may be only a few days between the appearance of typical mosaic symptoms on the vine tips and their death, leaving little or no indication of the cause.