PUBLICATION
Homologous tails? Or tales of homology?
- Authors
- McGhee, J.D.
- ID
- ZDB-PUB-000824-33
- Date
- 2000
- Source
- BioEssays : news and reviews in molecular, cellular and developmental biology 22(9): 781-785 (Review)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Caenorhabditis elegans
- DNA-Binding Proteins/genetics*
- Drosophila
- Evolution, Molecular*
- Fetal Proteins*
- Gene Expression Regulation, Developmental
- Male
- Mice
- Mutation*
- T-Box Domain Proteins/genetics
- Transcription Factors/genetics*
- PubMed
- 10944579 Full text @ Bioessays
Citation
McGhee, J.D. (2000) Homologous tails? Or tales of homology?. BioEssays : news and reviews in molecular, cellular and developmental biology. 22(9):781-785.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping