Abstract
Genetic analysis of the B2t locus has resulted in the recovery of four recessive mutations in the B2t structural gene and a deficiency that deletes the locus. Two of the mutations were recovered as suppressors of B2tD, a dominant male sterile mutation at the locus, and two were induced on wild-type chromosomes. All four mutant genes encode β2-tubulin subunits that are synthesized at normal rates but do not accumulate. All mutants are completely male sterile as homozygotes.
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Selected References
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