The Etl‐1 gene encodes a nuclear protein differentially expressed during early mouse development
Developmental Dynamics, ISSN: 1097-0177, Vol: 197, Issue: 3, Page: 227-237
1993
- 19Citations
- 24Captures
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- Citations19
- Citation Indexes19
- 19
- CrossRef17
- Captures24
- Readers24
- 24
Article Description
Recently, we isolated a novel mouse gene, Etl‐1 (Enhancer‐trap‐locus‐1), whose deduced amino acid sequence shows in its C‐terminal portion striking homology to the brahma protein (BRM), a transcriptional regulator of homeotic genes in Drosophila, and to SNF2/SWI2, a transcriptional regulator of various genes in Saccharomyces cerevisiae. Here we report the generation of antibodies against the Etl‐1 gene product (ETL‐1) and describe the subcellular localization as well as the expression and distribution of the ETL‐1 protein during mouse pre‐ and early post‐implantation development. ETL‐1 is a nuclear protein and is expressed in a biphasic manner during early embryogenesis. Moderate levels of ETL‐1 were detected in unfertilized and fertilized eggs but in the latter the protein was not concentrated in the pronuclei and seemed evenly distributed throughout the cytoplasm. In two‐cell embryos nuclear ETL‐1 protein accumulated transiently and levels decreased during subsequent cleavage development. After the morula stage, ETL‐1 levels increased again; in blastocysts high levels of ETL‐1 were present in inner cell mass cells whereas trophectoderm cells contained little or no ETL‐1. During subsequent development essentially all cell types except parietal endoderm and trophoblast cells contained high levels of ETL‐1. Our results imply that nuclear ETL‐1 is dispensable for the progression to the two cell stage, and suggest that during cleavage ETL‐1 might be needed at the onset of embryonic transcription. In blastocysts ETL‐1 function might be specifically required in cells of the inner cell mass and later in most cells of the embryo proper and extraembryonic ectoderm lineage. © 1993 Wiley‐Liss, Inc. Copyright © 1993 Wiley‐Liss, Inc.
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