Anti-AMELX (N-terminal) polyclonal antibody

Analysis of the sex of cattle meat by fast and reliable molecular techniques is an important measure to ensure correct allocation of export refunds, particularly in European countries and also in countries such as India where female cattle (cow) slaughter is banned legally in many areas because of religious beliefs. Based on the male-specific SRY gene, X and Y chromosome specific amelogenin gene 2 pair of primers was designed and the system of PCR was optimized. Upon PCR amplification, male tissue showed 3 bands, while female tissue resulted in only 1 band. The accuracy and specificity of the primers were assessed using DNA template extracted from cattle meat of known sex. The protocol was subjected to a blind test and showed 100% concordance, proving its accuracy and reliability.

Different mutations in the amelogenin gene (AMELX) result in the markedly different enamel phenotypes that are collectively known as amelogenesis imperfecta (AI). We hypothesize that unique phenotypes result from specific genetic mutations. The purpose of this study was to characterize the enamel compositional and structural features associated with a specific AMELX mutation in three families with X-linked Al. We performed mutational analysis by amplifying AMELX exons and sequencing the products. Permanent and primary affected (N = 6) and normal (N = 3) teeth were collected and examined by light, scanning, and transmission electron microscopy. Enamel proteins were evaluated by immunolocalization of amelogenin and amino acid analysis. AI-affected individuals all shared a common AMELX point mutation (C to A change at codon 41). The dental phenotypic findings were remarkably consistent in all affected individuals. The AI enamel was opaque, with numerous prism defects or holes encompassing the entire prism width. Affected crystallites appeared more radiolucent and morphologically less uniform, compared with that of normal enamel. Immunogold labeling with anti-amelogenin antibodies localized amelogenin to the crystallites but not to the inter-crystalline spaces. No immunogold labeling was seen in normal enamel. There was an increased and amelogenin-like protein content in AI enamel (0.95%) compared with normal enamel (0.13%). We conclude that this codon 41 C to A missense point mutation, in a highly conserved region of the AMELX gene, results in a remarkably consistent phenotype.