Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of a fish-specific genome duplication (FSGD) in the lineage leading to teleost fishes is widely accepted, but the consequences of this event remain elusive. Teleosts, and the cichlid fishes from the species flocks in the East African Great Lakes in particular, evolved a unique complexity and diversity of body coloration and color patterning. Several genes involved in pigment cell development have been retained in duplicate copies in the teleost genome after the FSGD. Here we investigate the evolutionary fate of one of these genes, the type III receptor tyrosine kinase (RTK) colony-stimulating factor 1 receptor (csf1r). We isolated and shotgun sequenced two paralogous csf1r genes from a bacterial artificial chromosome library of the cichlid fish Astatotilapia burtoni that are both linked to paralogs of the pdgfr beta gene, another type III RTK. Two pdgfr beta-csf1r paralogons were also identified in the genomes of pufferfishes and medaka, and our phylogenetic analyses suggest that the pdgfr beta-csf1r locus was duplicated during the course of the FSGD. Comparisons of teleosts and tetrapods suggest asymmetrical divergence at different levels of genomic organization between the teleost-specific pdgfr beta-csf1r paralogons, which seem to have evolved as coevolutionary units. The high-evolutionary rate in the teleost B-paralogon, consisting of csf1rb and pdgfr betab, further suggests neofunctionalization by functional divergence of the extracellular, ligand-binding region of these cell-surface receptors. Finally, we hypothesize that genome duplications and the associated expansion of the RTK family might be causally linked to the evolution of coloration in vertebrates and teleost fishes in particular.
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PMID:Asymmetric evolution in two fish-specifically duplicated receptor tyrosine kinase paralogons involved in teleost coloration. 1654 50

Epithelial cell proliferation, division, and differentiation are critical for barrier repair following inflammation, but the initial trigger for this process is unknown. Here we define that sensing of apoptotic cells by the TAM receptor tyrosine kinase Axl is a critical indicator for tracheal basal cell expansion, cell cycle reentry, and symmetrical cell division. Furthermore, once the pool of tracheal basal cells has expanded, silencing of Axl is required for their differentiation. Genetic depletion of Axl triggers asymmetrical cell division, leading to epithelial differentiation and ciliated cell regeneration. This discovery has implications for conditions associated with epithelial barrier dysfunction, basal cell hyperplasia, and continued turnover of dying cells in patients with chronic inflammatory pulmonary diseases.
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PMID:Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases. 3128 16