A Gut-to-Pharynx/Tail Switch in Embryonic Expression of the Caenorhabditis elegans ges-1 Gene Centers on Two GATA Sequences
| Autor: | Cheryl Van Buskirk, James D. McGhee, Mark F.P. Heschl, Fran L. Allen, May A. Chung, Cay Egan |
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| Rok vydání: | 1995 |
| Předmět: |
Genetic Markers
Tail Lineage (genetic) Molecular Sequence Data medicine.disease_cause Transformation Genetic medicine Animals Caenorhabditis elegans Promoter Regions Genetic Enhancer Molecular Biology Gene Psychological repression Genes Helminth Heat-Shock Proteins Sequence Deletion Regulation of gene expression Mutation Reporter gene Base Sequence Models Genetic biology Esterases Gene Expression Regulation Developmental Cell Biology DNA Helminth biology.organism_classification Molecular biology Intestines Enhancer Elements Genetic Phenotype Mutagenesis Site-Directed Pharynx Developmental Biology |
| Zdroj: | Developmental Biology. 170:397-419 |
| ISSN: | 0012-1606 |
| Popis: | The Caenorhabditis elegans ges-1 gene (gut es terase No. 1 ) is expressed only in the intestinal lineage, beginning when the developing gut has only four to eight cells. We analyze the sequence requirements for this tissue-specific gene regulation by injecting deleted/mutated constructs of the ges-1 gene into a viable ges-1 (null) strain of worms and assaying heritably transformed embryos by esterase histochemistry. Many deletion constructs accurately reconstitute the wildtype gut-specific ges-1 expression. However, deletions in the neighborhood of 1100 bp upstream of the ges-1 ATG abolish ges-1 expression in the developing gut, while at the same time activating ges-1 expression in cells of the pharynx/tail that appear to belong to the sister lineage of the gut. Deletions of a 36-bp DNA region containing two tandem WGATAR sequences are sufficient to cause this gut-to-pharynx/tail switch in expression pattern. Deletion of either one of the WGATAR sites or deletion of an adjoining downstream region directs ges-1 expression only in a restricted set of cells of the anterior gut. The ges-1 GATA region acts like a gut-specific enhancer in that: (i) it restores ges-1 gut expression when reinserted elsewhere into the GATA-deleted ges-1 gene; and (ii) multiple copies direct gut expression of an hsp16-lacZ reporter gene. The ges-1 GATA-region also acts as the site of the pharynx/tail repression in that reinsertion elsewhere into the GATA-deleted ges-1 construct causes repression of ges-1 in the pharynx/tail. However, multiple copies of the GATA region are not able to repress the heat-induced expression of an hsp 16-lacZ reporter gene, suggesting that the pharynx/tail repression mechanism is specific to the ges-1 environment. Finally, mutation rather than deletion of the individual GATA sequences suggests that gut activation and pharynx/tail repression may be due to separate factors. We present a molecular model that summarizes these results. The ges-1 control circuitry appears surprisingly complex for what might have been expected to be the simplest possible example of a nonessential gene expressed early in a clonal embryonic lineage. |
| Databáze: | OpenAIRE |
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