Myosin light-chain 1 and 3 gene has two structurally distinct and differentially regulated promoters evolving at different rates.

Abstract

DNA fragments located 10 kilobases apart in the genome and containing, respectively, the first myosin light chain 1 (MLC1f) and the first myosin light chain 3 (MLC3f) specific exon of the rat myosin light chain 1 and chicken shows that: (i) the MLC1f promoter regions have been highly conserved up to position -150 from the cap site while the MLC3f promoter regions display a very poor degree of homology and even the absence or poor conservation of typical eucaryotic promoter elements such as TATA and CAT boxes; (ii) the exon/intron structure of this gene has been completely conserved in the three species; and (iii) corresponding exons, except for the regions encoding most of the 5' and 3' untranslated sequences, show >75% homology while corresponding introns are similar in size but considerably divergent in sequence. The above findings indicate that the overall structure of the MLC1f/3f genes has been maintained between avian and mammalian species and that these genes contain two functional and widely spaced promoters. The fact that the structures of the alkali light chain gene from Drosophila melanogaster and of other related genes of the troponin C supergene family resemble a MLC3f gene without an upstream promoter and first exon strongly suggests that the present-day MLC1l13f genes of higher vertebrates arose from a primordial alkali light chain gene through the addition of a far-upstream MLC1rspecific promoter and first exon. The two promoters have evolved at different rates, with the MLC1f promoter being more conserved than the MLC3f promoter. This discrepant evolutionary rate might reflect different mechanisms of promoter activation for the transcription of MLCIf and MLC3f RNA.

A spliced Epstein-Barr virus gene expressed in immortalized lymphocytes is created by circularization of the linear viral genome.

“…Alternative 5' exons have been described in other systems, e.g. mouse a-amylase gene (Young et al, 1981), aldolase A (Joh et al, 1986), Thyl.2 cell surface glycoprotein (Ingraham and Evans, 1986) and myosin light chain gene (Strehler et al, 1985). A methione residue 63 nucleotides downstream of the 5' end of the 2.0 kb RNA is followed by a long open reading frame of 497 amino acids which spans eight of the nine exons.…”

Transcriptional regulation of the muscle creatine kinase gene and regulated expression in transfected mouse myoblasts.

“…Sevchicken a-actins (37,52), rat a-cardiac MHC (23), and the rat were made. First, at -400 nt and mouse myosin LC1 initiation regions (42,47), all at taining a perfect (interrupted) around -80 nt. The MCK gene does, however, contain a MOL.…”

“…Although these elements may not prove to be sufficient to allow expression of heterologous structural genes in muscle, their functional significance is suggested by their repeated appearance in close proximity to muscle-specific transcription initiation sites and by their conservation between chicken and rat DNAs. These elements do not, however, seem to be necessary for the expression of all musclespecific genes, since they are not found within the available upstream sequences of the myosin light-chain genes (36,42,47).…”

Developmentally regulated expression of a truncated myosin light-chain 1F/3F gene.

“…The existence of functional promoters for both MLC1f and MLC3f mRNAs has been demonstrated by in vitro studies (13) (1,9), exon 9 of the rat gene contains a sequence of 8 bases which is absent from the mouse gene (Fig. 2B).…”