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The Journal of Heredity 2000:91(4)
© 2000 The American Genetic Association 91:340-342

Brief communication. A new recessive ametapodia mutation in the chicken (Gallus domesticus

JR Smyth, Jr1,*, GP Sreekumar2, CA Coyle1, and JJ Bitgood3

1Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA 2Skin Biology Division, Johnson & Johnson, Skillman, NJ, USA 3University of Wisconsin, Madison, Wisconsin, USA *Corresponding author

An apparently new mutation that is associated with abnormal limb development appeared in a strain of Light Brown Leghorn chickens. Mutants are characterized by the complete absence of the tarsometatarsals, while severely hypoplastic development of the metacarpals is also present. The phenotype of the new mutant (ametapodia-2) closely resembles ametapodia-1, described in 1967, but ametapodia-2 is inherited as an autosomal recessive (AMET*A), while ametapodia-1 was associated with an incompletely dominant gene (MP*A). Only heterozygous ametapodia-1 (MP*N/MP*A were viable and able to reproduce, while homozygous ametapodia-2 mutants do not normally survive beyond 2-4 days of age. The shankless mutation (SHL*S) also reduces development of the metatarsal and metacarpal bones and has been shown to be associated with a pericentric inversion of chromosome 2. No obvious cytologic abnormality was apparent in ametapodia-2 birds, and offspring of a cross between AMET*A carriers and shankless birds were normal, indicating that the two mutations are not alleles. Ametapodia-1 (MP*A) was found to be linked to the rose comb locus (R) by 16 crossover units. Linkage test matings between AMET*A and (R*R) showed independent segregation, strongly suggesting that the mutation occurred at a relatively distant locus and therefore is probably not allelic to MP*A.


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