The Q gene is largely responsible for the widespread cultivation of wheat because it confers the freethreshing character. It also pleiotropically influences many other domestication-related traits such as glume shape and tenacity, rachis fragility, spike length, plant height, and spike emergence time. We isolated the Q gene and verified its identity by analysis of knockout mutants and transformation. The Q gene has a high degree of similarity to members of the AP2 family of transcription factors. The Q allele is more abundantly transcribed than q, and the two alleles differ for a single amino acid. An isoleucine at position 329 in the Q protein leads to an abundance of homodimer formation in yeast cells, whereas a valine in the q protein appears to limit homodimer formation. Ectopic expression analysis allowed us to observe both silencing and overexpression effects of Q. Rachis fragility, glume shape, and glume tenacity mimicked the q phenotype in transgenic plants exhibiting post-transcriptional silencing of the transgene and the endogenous Q gene. Variation in spike compactness and plant height were associated with the level of transgene transcription due to the dosage effects of Q. The q allele is the more primitive, and the mutation that gave rise to Q occurred only once leading to the world's cultivated wheats. W HEAT, rice, and maize are the three major cereal crops that provide most of the calories consumed by humans. Bread (common) wheat (Triticum aestivum L., 2n ¼ 6x ¼ 42, AABBDD genomes) arose 8000-10,000 years ago (for review see Nesbitt and Samuel 1996;Feldman 2001) from the spontaneous hybridization of the tetraploid wheat T. turgidum L. (2n ¼ 4x ¼ 28, AABB genomes) with the diploid goatgrass Aegilops tauschii Coss. (2n ¼ 2x ¼ 14, DD genomes) (Kihara 1944;McFadden and Sears 1946). Domestication of wheat resulted from mutations that gave rise to traits such as soft glumes, a nonfragile rachis, and the free-threshing character.The Q gene governs the free-threshing character and square spike phenotype. In addition, Q pleiotropically affects a repertoire of other characters important for domestication such as rachis fragility (Leighty and

To test the hypothesis that actin dysfunction leads to heart failure, patients with hereditary idiopathic dilated cardiomyopathy (IDC) were examined for mutations in the cardiac actin gene (ACTC). Missense mutations in ACTC that cosegregate with IDC were identified in two unrelated families. Both mutations affect universally conserved amino acids in domains of actin that attach to Z bands and intercalated discs. Coupled with previous data showing that dystrophin mutations also cause dilated cardiomyopathy, these results raise the possibility that defective transmission of force in cardiac myocytes is a mechanism underlying heart failure.

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