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Homologous tails? Or tales of homology?
Author(s) -
McGhee James D.
Publication year - 2000
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/1521-1878(200009)22:9<781::aid-bies2>3.0.co;2-8
Subject(s) - brachyury , biology , gene , genetics , mutant , phenotype , homology (biology) , zebrafish , locus (genetics) , hindgut , embryonic stem cell , midgut , mesoderm , botany , larva
Classical mutations at the mouse Brachyury ( T ) locus were discovered because they lead to shortened tails in heterozygous newborns. no tail ( ntl ) mutants in the zebrafish, as their name suggests, show a similar phenotype. In Drosophila , mutants in the brachyenteron ( byn ) gene disrupt hindgut formation. These genes all encode T‐box proteins, a class of sequence‐specific DNA binding proteins and transcription factors. Mutations in the C . elegans mab‐9 gene cause massive defects in the male tail because of failed fate decisions in two tail progenitor cells. In a recent paper, Woollard and Hodgkin(1) have cloned the mab‐9 gene and found that it too encodes a T‐box protein, similar to Brachyury in vertebrates and brachyenteron in Drosophila . The authors suggest that their results support models for an evolutionarily ancient role for these genes in hindgut formation. We will discuss this proposal and try to decide whether the gene sequences, gene interactions and gene expression patterns allow any conclusions to be made about the rear end of the ancestral metazoan. BioEssays 22:781–785, 2000. © 2000 John Wiley & Sons, Inc.

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