Corn (Zea mays) is widely cultivated for human food and animal feed and also provides an ecosystem service as a trap crop for the corn earworm Helicoverpa zea (Boddie) (Lepidoptera: Noctuidae) in tomato cropping systems. To be able to use corn as a trap crop for H. zea and to prevent it turning into a source of infestation, varieties are needed that are both attractive and resistant to H. zea. The main objective of this study was to compare the attractiveness to oviposition by H. zea and the resistance to H. zea of 10 sweet corn varieties in field conditions. We found Java, Garrison, Nova and Shinerock varieties that were both attractive to H. zea with a similar or higher number of eggs laid on silks than in the susceptible corn varieties, and resistant to H. zea, with fewer larvea per ear than in susceptible corn varieties. These varieties provide favorable habitats for generalist predators, ants, spiders, minute pirate bugs and lady beetles, which may account for their "dead-end" properties. Tropical farmers now have sweet corn varieties that can serve both as cash crops and as trap crops for H. zea.
The diagnosis of rare inherited diseases is becoming more and more complex as an increasing number of clinical conditions appear to be genetically heterogeneous. Multigenic inheritance also applies to the autosomal recessive progressive cerebellar ataxias (ARCAs), for which 14 genes have been identified and more are expected to be discovered. We used homozygosity mapping as a guide for identification of the defective locus in patients with ARCA born from consanguineous parents. Patients from 97 families were analyzed with GeneChip Mapping 10K or 50K SNP Affymetrix microarrays. We identified six families homozygous for regions containing the autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) gene, two families homozygous for the ataxia-telangiectasia gene (ATM), two families homozygous for the ataxia with oculomotor apraxia type 1 (AOA1) gene, and one family homozygous for the AOA type 2 (AOA2) gene. Upon direct gene testing, we were able to identify a disease-related mutation in all families but one of the two kindred homozygous at the ATM locus. Although linkage analyses pointed to a single locus on chromosome 11q22.1-q23.1 for this family, clinical features, normal levels of serum alpha-foetoprotein as well as absence of mutations in the ATM gene rather suggest the existence of an additional ARCA-related gene in that interval. While the use of homozygosity mapping was very effective at pointing to the correct gene, it also suggests that the majority of patients harbor mutations either in the genes of the rare forms of ARCA or in genes yet to be identified.
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