A dinucleotide repeat in the mouse biglycan gene (EST) on the X Chromosome

Rau, W.; Just, Walter; Vetter, U.; Vogel, Walther

doi:10.1007/bf00356564

Cited by 7 publications

(2 citation statements)

References 11 publications

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“…A 1 kbp Bam HI– Sac I fragment contained part of intron 1, exon 1, and ∼550 bp 5′ sequence. Comparisons were made to the mouse biglycan cDNA sequence31 and the human gene 6. With few exceptions, the 5′ sequence was identical to the sequence recently published32 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Functional Characterization of the Human Biglycan 5′-Flanking DNA and Binding of the Transcription Factor c-Krox

Heegaard

Robey

Vogel

et al. 1997

Journal of Bone and Mineral Research

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The transcriptional regulation of human biglycan expression under normal and pathological conditions was studied. The 5-flanking regions of the human and mouse genes were isolated and analyzed; the two promoter regions share 81% identity. Both promoters are without a TATA and CAT box and contain multiple Sp1 sites. Human dermal fibroblasts were transiently transfected with progressive deletional human biglycan 5-flanking DNA-CAT constructs, and a significant variation in activity among the individual constructs was found. A small deletion in several cases caused a more than 2-fold increase or decrease in promoter activity, thereby mapping the target sites for repressors or activators. Human biglycan expression is reduced in females with Ullrich-Turner syndrome (45,X) and increased in individuals with supernumerary sex chromosomes, and it has been speculated that biglycan plays a role in the short stature phenotype of Turner syndrome. Analysis of the transcriptional regulation of biglycan in individuals with sex chromosome anomalies showed that a -262 to -218 region of the biglycan promoter was differentially regulated. This region was extensively analyzed by DNAse footprinting and electrophoretic mobility shift assays, and a putative binding site for the transcription factor c-Krox was discovered. The binding of c-Krox to a site located at approximately -248 to -230 in the human biglycan promoter was confirmed by using extracts from COS cells expressing recombinant human c-Krox. The expression of c-Krox in bone was then examined by reverse-transcribed polymerase chain reaction and Northern blotting analysis; an ϳ3.4 kb transcript was detected in primary osteoblastic cells, in MG-63 cells, and in human bone marrow stromal cells. This is the first detection of c-Krox in bone cells, and it suggests that c-Krox, like another member of the Krox family, Krox-20, might play a regulatory role in

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Section: Resultsmentioning

confidence: 99%

Functional Characterization of the Human Biglycan 5′-Flanking DNA and Binding of the Transcription Factor c-Krox

Heegaard

Robey

Vogel

et al. 1997

Journal of Bone and Mineral Research

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“…There is a (CA) dinucleotide repeat in the 3)UTR of the X chromosomal biglycan gene Rau et al, 1994). We cloned this fragment from Ellobius lutescens, determined its sequence and specific primers.…”

Section: Pcr Markers On the X Chromosome Of Ellobius Lutescensmentioning

confidence: 99%

Sex determination in <i>Ellobius lutescens:</i> The story of an enigma

Vogel

Jainta

Rau

et al. 1998

Cytogenet Genome Res

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The unusual karyotype of Ellobius lutescens (2n = 17,X in males and females) has attracted permanent interest and prompted a series of hypotheses on sex determination in this species since its first description by Matthey (1953). The developing knowledge about the sex chromosomes and sex determination as well as the availability of new cytogenetic and molecular genetic techniques prompted studies to test the compatibility between current hypotheses and new findings and rendered modifications of the hypotheses necessary. After a long period dominated by the question what the sex chromosome constitution of this species might be and where the testis determining factor could be located, the presence of Sry had been eventually excluded and sex determination attributed to a hypothetical mutated gene acting downstream of Sry. An X-chromosomal or autosomal location of this gene can be assessed by cosegregation of sex with X-chromosome markers. Some preliminary results concerning X-chromosome dinucleotide repeat markers are reported. However, these markers were homomorphic in Ellobius lutescens. We now report evidence that Zfy is also missing in Ellobius lutescens and E. tancrei (males and females XX), a finding from which we conclude that the entire Y chromosome has been lost from these species. Perspectives concerning future studies are discussed.

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