Cranberry stem gall is characterized by tumors that girdle stems, thereby killing all distal leaves, flowers, and fruit. Bacteria that produce high levels of the plant growth hormone indole-3-acetic acid (IAA) are associated with and believed to cause cranberry stem gall. The anatomy of naturally occurring galls on woody cranberry plants and galls caused by inoculation of micropropagated cranberry plants with Pantoea agglomerans strain 4/99 was consistent with elevated levels of IAA in plants. Field galls exhibited hypertrophy and hyperplasia of tissue external to the vascular cambium, resulting in extensive stem swelling and splitting of the periderm. Similarly, galls on micropropagated plants contained enlarged cortical parenchyma cells. The current year's xylem vessels in field galls were narrow and dense compared with xylem vessels of healthy stems. Curved xylem elements apparently developed de novo within field galls and galls on inoculated plants. Cavities and fissures in both types of galls contained dense aggregates of bacteria. Treatment of micropropagated plants with synthetic IAA caused hypertrophy of cortical parenchyma and formation of adventitious roots. The results support the hypothesis that IAA-producing bacteria cause cranberry stem gall.

Two sampling strategies were compared and sources of variability in the sampling protocols analyzed to optimize sampling methods for studies of cranberry fruit rot that occurs in the field (i.e., field rot). For the first method, fruit were dry picked by hand from randomly assigned quadrats; for the second method, fruit were scooped from harvest floodwaters. Rot incidence, which ranged from 1.8 to 9.7%, did not differ significantly between upland and lowland sites or, in general, between dry-picked and wet-harvested samples. There were no consistent differences between upland and lowland sites in the frequency of isolation of any fungus from either rotten or sound fruit. The incidence of certain saprophytic and soilborne fungi was greater in wet-harvested compared with dry-picked fruit. In general, rot incidence and incidence of various fungal taxa isolated from fruit varied more among samples within sites than among sites. Site type (i.e., upland or lowland) was never a major source of variability. These findings suggest that if the goal were to assess the occurrence of cranberry fruit rot within a region, intensive within-site sampling would be necessary, but site type would not be an important consideration, at least in Wisconsin, where this study was conducted.

The efficacy of fungicides in controlling cottonball disease of cranberry was tested during 1996 to 1998 at three locations in Wisconsin. For some fungicides, the efficacy of four applications, two each during shoot elongation and bloom, was compared with two applications during bloom only. Spraying twice during bloom was as effective in controlling secondary infection as spraying twice during shoot elongation plus twice during bloom. Azoxystrobin, cyprodinil, and propiconazole were equally effective. None of the treatments affected yield, fruit retention, or berry weight compared with the controls. Sensitivity of M. oxycocci, the cottonball pathogen, to fenbuconazole and propiconazole was tested in vitro by comparing the distributions of ED50 values of populations collected from three sites that differed in previous exposure to fungicides. Median ED50 values for fenbuconazole were significantly greater at sites where sterol demethylation inhibitor fungicides had been used compared with a site where fungicides had never been used, but median ED50 values for propiconazole did not differ among sites. There was no correlation between the sensitivities to fenbuconazole and propiconazole. The data will form the basis of recommendations aimed at delaying the onset of fungicide resistance and will provide a baseline for monitoring resistance to fenbuconazole and propiconazole in populations of M. oxycocci in the future.

Plants were regenerated from callus cultures of maize inbred W182BN with the S(USDA) type of cytoplasmic male sterility (cms). Some regenerates from 16 of 18 separate cultures had fertile tassels. Many other regenerates, whose fertility could not be scored accurately because of abnormal plant morphology, produced fertile progeny after pollination with N cytoplasm W182BN. Revertant plants and/or progeny were obtained from all 18 cultures, which included the CA, D, LBN, and S sources of cmsS. More revertants were recovered from cultures maintained as callus for 12 months than from 3-4 month old cultures. Several types of evidence (absence of segregation for fertility after selfing or pollination of revertants with standard W182BN, pollen viability counts, failure of revertants to restore sterile cmsS lines to fertility, mitochondrial DNA analyses) indicated that the reversion to fertility involved cytoplasmic rather than nuclear alterations. All revertants examined lacked the S1 and S2 plasmid-like DNAs characteristic of the mitochondrial genome of sterile cmsS lines. Most callus cultures lost S1 and S2 after 13-20 months in vitro. No revertants were seen among thousands of W182BN cmsS plants grown from seed in the field or among plants from tissue cultures of W182BN with the C or T types of cms. The cytoplasmic revertants recovered from culture may be useful for the molecular analysis of cmsS.

Infection of cranberry flowers by conidia of Monilinia oxycocci, the cottonball pathogen, was investigated using a squash-mount histological method. Conidia germinated on anthers, nectaries, petals, and stigmata, but not styles. The stigma was the only flower part penetrated by the fungus, but no specialized infection structures were noted. Both fungal and pollen germ tubes grew through the stylar canal and made contact with ovules and nucellar tissue by 72 h after inoculation and pollination. Cottonball incidence was greatest when stigmata were inoculated; the low level of cottonball that resulted from inoculation of other flower parts and in noninoculated flowers was attributed to contamination of stigmata. In greenhouse tests, cottonball incidence was 25, 28, 31, and 38% for cvs. Searles, Pilgrim, Ben Lear, and Stevens, respectively, and was greater for M. oxycocci isolate 593 than isolate 591. We conclude that the stigma is the sole floral infection court for conidia of M. oxycocci and that the most popular cranberry cultivars in Wisconsin do not differ in inherent resistance to cottonball. The relevance of these findings to the long-term management of cottonball is discussed.