CpG islands in vertebrate genomes.

https://www.cell.com/cell/pdf/0092-8674(87)90151-6.pdf

Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

The c-myc gene product is a nuclear protein1,2 expressed in a wide variety of cell types3. It has been implicated in the control of normal cell growth as well as transformation4–7, but its exact function is unknown. When the human promyelocytic leukaemia cell line HL60 is treated with retinoic acid, the cells differentiate into granulocytes, and there is a reduction in steady state c-myc RNA of more than 10-fold8. Nuclear runoff assays show that this reduction is caused by a corresponding decrease in the transcription of exon 2. However, only a minor decrease in exon 1 transcription is observed upon differentiation. In undifferentiated HL60 cells there is an approximately 3-fold molar excess of exon 1 transcription over exon 2, and this excess increases to about 15-fold in differentiated cells. This observation suggests that a major component of c-myc transcriptional down-regulation in HL60 cells is at the level of elongation rather than at the level of initiation. The position of the elongation block was mapped to the region of the boundary between exon 1 and intron 1. During HL60 differentiation, a DNase I hypersensitive site in the chromatin about 300 bases downstream of the 5′ end of of intron 1 increases in intensity relative to other sites, possibly reflecting events associated with the termination of transcription. Our runoff analysis also revealed transcription of both strands immediately upstream of exon 1 in HL60 cells. The sense strand transcription of this region produces a novel c-myc RNA which initiates several hundred bases upstream of the previously defined promoters and is found in a variety of cell types.

A block to elongation is largely responsible for decreased transcription of c-myc in differentiated HL60 cells.

Molecular analysis of mbcl-2: Structure and expression of the murine gene homologous to the human gene involved in follicular lymphoma

https://www.cell.com/cell/pdf/0092-8674(88)90257-7.pdf

The human X-linked steroid sulfatase gene and a Y-encoded pseudogene: evidence for an inversion of the Y chromosome during primate evolution.

Theuseofmurine dihydrofolate reductase (dhfr) geneamplification mutants enabled ustoidentify important structural andfunctional features ofthedhfr promoter region. We foundanother transcription unit, atleast 14kilobases insize, whichinitiates within 130basepairs ofthemajor dhfrtranscript andistranscribed divergently. The5'endsofbothtranscripts wereanalyzed andfoundtohavemultiple initiation sites. The major dhfrtranscript andthedivergent transcript appear toshare thesamepromoter region; thelonger transcripts ofthedhfr geneoverlap withthedivergent transcripts anduseadifferent promoter region. The divergent transcript appears tocodeforaprotein; anhomologous sequence toitsfirst exonisfoundinthe corresponding location nearthehumandhfr gene. Mostcellular generegulation studies havebeenconcerned with genes that codeforproteins produced inlarge quantities inspecific typesofterminally differentiated cells. A large bodyofevidence indicates that theexpression ofsuchgenes iscontrolled transcriptionally (10). However, manycellular genes, perhaps most, codeforenzymes which arepresent at lowlevels invirtually all types ofcells. Studies concerning theexpression ofhousekeeping enzymes orproteins suchas dihydrofolate reductase (dhfr; 17,20,21), thymidine kinase (15), tubulin (7,16), andglyceraldehyde-3-phosphate dehydrogenase (29)indicate thatthedifferential expression of these genesseenasafunction ofcell growth orseenin different tissues iscontrolled posttranscriptionally. Thus,

Analysis oftheMousedhfr Promoter Region: Existence ofa Divergently Transcribed Gene

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Analysis oftheMousedhfr Promoter Region: Existence ofa Divergently Transcribed Gene