The Alu Yc1 subfamily: sorting the wheat from the chaff.

Members of the Alu Yc1 subfamily are distinguished from the older Alu Y subfamily by a signature G-->A substitution at base 148 of their 281-bp consensus sequence. Members of the much older and larger Alu Y subfamily could have by chance accumulated this signature G-->A substitution and be misclassified as belonging to the Alu Yc1 subfamily. Using a Mahanalobis classification method, it was estimated that the "authentic" Alu Yc1 subfamily consists of approximately 262 members in the human genome. PCR amplification and further analysis was successfully completed on 225 of the Yc1 Alu family members. One hundred and seventy-seven Yc1 Alu elements were determined to be monomorphic (fixed for presence) in a panel of diverse human genomes. Forty-eight of the Yc1 Alu elements were polymorphic for insertion presence/absence in diverse human genomes. The insertion polymorphism rate of 21% in the human genome is similar to rates reported previously for other "young" Alu subfamilies. The polymorphic Yc1 Alu elements will be useful genetic loci for the study of human population genetics.

Alu insertion polymorphisms for the study of human genomic diversity.

Genomic database mining has been a very useful aid in the identification and retrieval of recently integrated Alu elements from the human genome. We analyzed Alu elements retrieved from the GenBank database and identified two new Alu subfamilies, Alu Yb9 and Alu Yc2, and further characterized Yc1 subfamily members. Some members of each of the three subfamilies have inserted in the human genome so recently that about a one-third of the analyzed elements are polymorphic for the presence/absence of the Alu repeat in diverse human populations. These newly identified Alu insertion polymorphisms will serve as identical-by-descent genetic markers for the study of human evolution and forensics. Three previously classified Alu Y elements linked with disease belong to the Yc1 subfamily, supporting the retroposition potential of this subfamily and demonstrating that the Alu Y subfamily currently has a very low amplification rate in the human genome.

Formation of Sclerotia and Aflatoxins in Developing Cotton Bolls Infected by the S Strain of Aspergillus flavus and Potential for Biocontrol with an Atoxigenic Strain.

ABSTRACT Aspergillus flavus can be divided into the S and L strains on the basis of sclerotial morphology. On average, S strain isolates produce greater quantities of aflatoxins than do L strain isolates. Sclerotia of the S strain were observed in commercial seed cotton from western Arizona. Greenhouse tests were performed to better define sclerotial formation in developing bolls. Eight S strain isolates were inoculated into developing bolls via simulated pink bollworm exit holes. All eight isolates formed sclerotia on locule surfaces, and seven of eight isolates produced sclerotia within developing seed. Boll age at inoculation influences formation of sclerotia. More sclerotia formed within bolls that were less than 31 days old at inoculation than in bolls older than 30 days at inoculation. Frequent formation of sclerotia during boll infection may both favor S strain success within cotton fields and increase toxicity of A. flavus-infected cottonseed. Atoxigenic A. flavus L strain isolate AF36 reduced formation of both sclerotia and aflatoxin when coinoculated with S strain isolates. AF36 formed no sclerotia in developing bolls and was more effective at preventing S strain isolates than L strain isolates from contaminating developing cottonseed with aflatoxins. The use of atoxigenic L strain isolates to prevent contamination through competitive exclusion may be particularly effective where S strain isolates are common. In addition to aflatoxin reduction, competitive exclusion of S strain isolates by L strain isolates may result in reduced overwintering by S strain isolates and lower toxicity resulting from sclerotial metabolites.