ABSTRACT
LpS1 RNA transcripts and proteins are expressed exclusively in the aboral ectoderm of the embryo in the sea urchin Lytechinus pictus. We have characterized the LpS1-beta promoter to identify the cis-acting elements that may be involved in the aboral ectoderm-specific expression of the LpS1-beta gene. The distal G-string site, composed of six contiguous guanine deoxynucleotides located at -721 to -726, was analyzed. A mutation at the distal G-string caused over a two-fold increase in reporter chloramphenicol acetyltransferase gene activity and inappropriate expression of reporter green fluorescent protein in nonaboral ectoderm cells in L. pictus embryos. These results suggest that the proteins that bind the distal G-string act as a spatial repressor in the nonaboral ectoderm cells of the developing embryo.
Subject(s)
Calcium-Binding Proteins/genetics , Gene Expression Regulation, Developmental/genetics , Promoter Regions, Genetic/genetics , Repressor Proteins/metabolism , Sea Urchins/genetics , Transcription Factors/genetics , Animals , Base Sequence , Binding Sites , Chloramphenicol O-Acetyltransferase/biosynthesis , Chloramphenicol O-Acetyltransferase/genetics , DNA/metabolism , DNA, Recombinant , Ectoderm , Embryo, Nonmammalian , Genes, Reporter/genetics , Green Fluorescent Proteins , Luminescent Proteins/biosynthesis , Luminescent Proteins/genetics , Molecular Sequence Data , Mutation , Sea Urchins/embryologyABSTRACT
The Nagase analbuminemic rat (NAR), a mutant of the Sprague-Dawley (SD) strain, exhibits persistent hypercholesterolemia, thrombocytosis, and enhanced platelet aggregation, abnormalities possibly involved in the genesis of glomerular sclerosis (GS). Previous observations suggest that these rats never develop aging GS. We studied the development of GS in NAR after 5/6 nephrectomy (Nx). Fifteen days after Nx, marked glomerular hypertension was observed in NAR, compared with only mild elevations in SD rats. Glomerular hypertrophy was more marked in SD rats than in NAR. Enalapril normalized glomerular volume and partially reversed glomerular hypertension in NAR without altering platelet function or cholesterol levels. Glomerular endothelial injury and intraluminal fibrin deposition were seen only in NAR. Two months after Nx, severe GS and massive glomerular lipid deposition were seen in NAR, whereas only mild glomerular injury occurred in SD rats. Enalapril attenuated GS and prevented lipid deposition in NAR. Glomerular hypertension may be a key factor in the genesis of GS in this model in association with endothelial injury, intracapillary coagulation, and lipid accumulation.
