Cell Adhesion Complex Research Articles

Isolation and characterization of a human pseudogene (CTNNAP1) for αE-catenin (CTNNA1): assignment of the pseudogene to 5q22 and the αE-catenin gene to 5q31

A pseudogene (CTNNAP1) for the human αE-catenin gene was isolated from a human genomic phage library. The pseudogene sequence shows 90% similarity to the αE-catenin mRNA at the nucleotide level. Thirty-eight stop codons in all three reading frames and multiple other mutations were found, indicating that the pseudogene does not encode a functional protein. No introns were found in the region corresponding to the open reading frame of the αE-catenin cDNA, and two direct repeats flank this same region. Hence, the pseudogene can be classified as a processed pseudogene. Polymerase chain reaction with pseudogene-specific primers on genomic DNA and cDNA from human cell lines and healthy blood donors demonstrated the general occurrence of the pseudogene and the lack of its transcription. By fluorescence in situ hybridization the pseudogene was mapped to human chromosome 5q22 and the αE-catenin gene to the formerly disputed locus 5q31. This is the first report of a pseudogene for a member of the cadherin—catenin cell—cell adhesion complex.

Cloning of the Human α-Catenin cDNA and Its Aberrant mRNA in a Human Cancer Cell Line

Cadherin and catenin compose cell adhesion complex and are indispensable for tight cell-cell adhesion. Dysfunction of this adhesion complex causes dissociation of cancer cells from primary tumor nodules, thus possibly contributing to cancer invasion and metastasis. In this report, we present the human α-caienin sequence. Human α-catenin showed extensive homology with that of mouse, i.e., 91.8% and 99.3% at the nucleic acid and amino acid levels, respectively, indicating that this molecule has been evolutionarily conserved in mammals. Characterization of the mRNA sequence of α-catenin in PC9 was also carried out, and two distinct abnormal sequences, i.e.,one of 957 bp deletion resulting in a 319-amino-acid deletion and another of 761 bp deletion resulting in a frameshift, were identified. These deletions were probably produced by an error of RNA splicing, presenting one possible mechanism for the loss of intact α-catenin expression.