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R Flegg

Publications and source records attributed to R Flegg.

3 recordsLinked to original sources
PubMed1997

The mouse Plk gene: structural characterization, chromosomal localization and identification of a processed Plk pseudogene.

The Plk gene encodes a serine/threonine protein kinase believed to be important for the normal progression of mammalian cells through the cell cycle. In this paper, we report the genomic organization of the mouse Plk gene. The mouse Plk gene encompasses 16 kb of the mouse genome and is organised into 10 exons. Based on homology with the human PLK1 promoter region, the putative mouse promoter region includes a CCAAT motif but lacks the conventional TATA motif. The proposed promoter region contains consensus binding sites for several transcriptional regulators, including Sp1 and AP2. In addition to the active copy of Plk, Plk exists as a processed pseudogene. Using RFLP analysis, we have localized the active Plk gene to mouse Chromosome 7 and the processed pseudogene to mouse Chromosome 5. Southern blot analysis of DNA from a limited number of other mammalian species suggests that the duplication is confined to the mouse. Parsimony analysis suggests that the gene duplication leading to the mouse Plk pseudogene occurred after the rat-mouse split.

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PubMed1997

Microsatellite deletions in the c-myb transcriptional attenuator region associated with over-expression in colon tumour cell lines.

In the hemopoietic system c-myb expression is required for proliferation of immature cells and its down-regulation is required for differentiation. In colonic mucosa c-myb expression occurs at levels comparable to immature hemopoietic cells. Inhibition of c-myb expression in colon cell lines, using anti-sense oligonucleotides, indicates that c-myb expression is required for proliferation. However, the mechanism of c-myb regulation during colon cell differentiation has not been explored. Using the LIM1215 and CaCo-2 colon carcinoma cell lines induced to differentiate with sodium butyrate, we demonstrate that c-myb mRNA is down-regulated as an early event in differentiation by a mechanism involving transcriptional attenuation in intron 1. By analogy with procaryotic and eucaryotic genes, transcriptional attenuation probably occurs in a region containing nineteen consecutive thymidine residues. Computer prediction of the secondary structure of the nascent mRNA chain encoded by this region suggests a strong potential for stem-loop formation. Sequence analysis of several colon tumour cell lines reveals mutations in this region that may disrupt transcriptional attenuation and result in the increased c-myb expression observed in colon tumours and tumour cell lines.

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