Temperature, leaf wetness, and isolate effects on infection of Minneola tangelo leaves by Alternaria sp.

Alternaria brown spot causes necrotic lesions on immature leaves, twigs, and fruit of tangerines and their hybrids, reducing yield and fruit quality. The effect of temperature, leaf wetness, and isolate was evaluated in an in vitro system using immature detached leaves of Minneola tangelo. Infection was greatest at 27°C, decreased gradually as the temperature declined to 24, 20, and 17°C, and dropped sharply at 32°C. Levels of infection were low at 4 and 8 h of leaf wetness and continued to increase with longer wetting periods up to 36 h. A polynomial equation was developed that provided a good fit for the data (adjusted R2 = 0.93). Isolates differed in aggressiveness, but there was no significant difference among isolates in their response to temperature and leaf wetness duration

Population genetic structure and host specificity of Alternaria spp. causing brown spot of Minneola tangelo and rough lemon in Florida

Alternaria spp. were sampled from two rough lemon (RL) and two Minneola tangelo (MIN) groves in a limited geographic area in central Florida to test for host-specialized forms of the pathogen. Isolates of Alternaria spp. were scored for variation at 16 putative random amplified polymorphic DNA (RAPD) loci and for pathogenicity on both hosts. Subpopulations on each host were differentiated genetically and pathogenically, which was consistent with the hypothesis of host specialization. Highly significant genetic differentiation was detected among all four subpopulations (Nei's coefficient of gene differentiation [G(ST)] = 0.292, P = 0.000); most of the differentiation occurred between hosts (G(ST) = 0.278, P = 0.000). Phenograms of qualitative similarities among isolates within subpopulations revealed two or three distinct clusters of isolates within each subpopulation. The majority of isolates sampled from RL were pathogenic on RL and not on MIN, although a few RL isolates were able to induce disease on MIN, and 44% were nonpathogenic on either host. In contrast, isolates from MIN were pathogenic only on MIN, never on RL, and only 3% of the isolates were nonpathogenic. Overall, three genetically distinct clusters of isolates were detected on both hosts. One of the clusters (cluster A) sampled from RL was pathogenic on RL and not on MIN and consisted almost entirely of one RAPD genotype. This cluster also contained two isolates that were 93% similar to the majority genotype but were pathogenic on MIN and not RL. In isolates from MIN, two distinct clusters of isolates were found in one subpopulation (clusters B and C), and three distinct clusters were found in another subpopulation (clusters A, B, and C). Clusters A and B were found on both hosts, while cluster C was limited to MIN. Populations of Alternaria spp. sampled from RL and MIN showed a high degree of host specificity; however, the specificity obscured a high level of genetic variation within subpopulations