Mouse annexin V genomic organization includes an endogenous retrovirus

RODRIGUEZ-GARCIA, Maria-Isabel; Morgan, Reginald O.; Bances, Patricia; Fernández, Mónica

doi:10.1042/0264-6021:3370125

Cited by 8 publications

(12 citation statements)

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“…A 6-kb retroviral insertion was detected in intron 2 of the mouse. Although unusual, this need not impair gene function because in at least one other instance (a mouse annexin gene), a complete retroposon sequence is efficiently spliced out of an intron (43). The mouse and rat AADA genes reported here appear in all other respects to be functional because mutations have not accumulated in the coding sequences, the untranslated regions, or the splice sites.…”

Section: Table IV Effects Of Fibrates On Hepatic and Intestinal Levelmentioning

confidence: 94%

Characterization of the Rodent Genes for Arylacetamide Deacetylase, a Putative Microsomal Lipase, and Evidence for Transcriptional Regulation

Trickett¹,

Patel²,

Knight³

et al. 2001

Journal of Biological Chemistry

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In the current study, we have determined the cDNA and the genomic sequences of the arylacetamide deacetylase (AADA) gene in mice and rats. The AADA genes in the rat and mouse consist of five exons and have 2.4 kilobases of homologous promoter sequence upstream of the initiating ATG codon. AADA mRNA is expressed in hepatocytes, intestinal mucosal cells (probably enterocytes), the pancreas and also the adrenal gland. In mice, there is a diurnal rhythm in hepatic AADA mRNA concentration, with a maximum 10 h into the light (post-absorptive) phase. This diurnal regulation is attenuated in peroxisome proliferator-activated receptor ␣ knockout mice. Intestinal but not hepatic AADA mRNA was increased following oral administration of the fibrate, Wy-14,643. The homology of AADA with hormone-sensitive lipase and the tissue distribution of AADA are consistent with the view that AADA plays a role in promoting the mobilization of lipids from intracellular stores and in the liver for assembling VLDL. This hypothesis is supported by parallel changes in AADA gene expression in animals with insulin-deficient diabetes and following treatment with orotic acid.

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Section: Table IV Effects Of Fibrates On Hepatic and Intestinal Levelmentioning

confidence: 94%

Characterization of the Rodent Genes for Arylacetamide Deacetylase, a Putative Microsomal Lipase, and Evidence for Transcriptional Regulation

Trickett¹,

Patel²,

Knight³

et al. 2001

Journal of Biological Chemistry

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“…Interestingly, a LINE-2 element with transcriptionally repressive components has been characterized in the upstream promoter of annexin A6 [27], with which annexin A5 shared its most recent common ancestor [43]. A complete murine endogenous retroviral element (MuERV)-L resides in mouse annexin A5 intron 4 [20], and a rare Alu subfamily retroposon at bp k452 to k627 in the human annexin A1 promoter [24], further testify to the involvement of retroposons in the structural evolution of annexin genes.…”

Section: Discussionmentioning

confidence: 99%

“…Primer extension analysis of annexin A5, using tissue RNA samples as template for reverse transcription, previously demonstrated a heterogenous pattern of extension bands [10,20], indicating that gene transcription may initiate at multiple sites. Plasmid constructs containing 5h and 3h serial deletions of the predicted promoter regulatory region were made to further assess the start site variability and to localize regions responsible for transcriptional activity.…”

Section: Initiation Of Transcription In the Human Annexin A5 Genementioning

confidence: 99%

“…annexin A5 orthologues from human [10], rat [19], mouse [20] and chick [21] have helped to identify conserved regulatory motifs and coding regions with implied roles ; however, the functionally active domains remain to be characterized. The localization of essential cis-acting genomic elements and the identification of trans-acting protein factors involved in annexin A5 gene expression are requisite to understanding the molecular control mechanisms for this and related genes, and may shed light on their possible involvement in tissue-specific growth and differentiation.…”

Section: Introductionmentioning

confidence: 99%

“…annexin A1 in pigeon [22] and human [23][24][25][26] and those for human annexins A6 [26,27] and A7 [28]. Annexins A5 and A6 shared their most recent common ancestor 500-700 million years ago [20], yet they retain no apparent homology in noncoding regions. Although both gene promoters lack a TATA box or initiator element and have GC-rich regions containing putative Sp1 binding elements, annexin A5 exhibits marked differences in its initiation of transcription at multiple start sites and from an alternative, noncoding exon 1a in rat nervous tissues [19].…”

Section: Introductionmentioning

confidence: 99%

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Functional analysis of the human annexin A5 gene promoter: a downstream DNA element and an upstream long terminal repeat regulate transcription

Carcedo

Iglesias

Bances

et al. 2001

Biochemical Journal

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Human annexin A5 is a ubiquitous protein implicated in diverse signal transduction processes associated with cell growth and differentiation, and its gene regulation is an important component of this function. Promoter transcriptional activity was determined for a wide 5′ portion of the human annexin A5 gene, from bp −1275 to +79 relative to the most 5′ of several discrete transcription start points. Transfection experiments carried out in HeLa cells identified the segment from bp −202 to +79 as the minimal promoter conferring optimal transcriptional activity. Two canonical Sp1 sites in the immediate 5′ flanking region of a CpG island were required for significant transcription. Strong repressive activity in the distal promoter region between bp −717 to −1153 was attributed to the presence of an endogenous retroviral long terminal repeat, homologous with long terminal repeat 47B. The downstream sequence from bp position +31 to +79 in untranslated exon 1 was also essential for transcription, as its deletion from any of the plasmid constructs abolished activity in transfection assays. Electrophoretic mobility-shift assays, Southwestern-blot analysis and affinity chromatography were used to identify a protein doublet of relative molecular mass 35kDa that bound an octanucleotide palindromic sequence in exon 1. The DNA cis-element resembled an E-box, but did not bind higher molecular mass transcription factors, such as upstream stimulatory factor or activator protein 4. The discovery of a downstream element crucial for annexin A5 gene transcription, and its interaction with a potentially novel transcription factor or complex, may provide a clue to understanding the initiation of transcription by TATA-less, multiple start site promoters.

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Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

Turnay

Olmo

Lizarbe

et al. 2001

J of Cellular Biochemistry

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Several lines of evidence indicate that annexin A5, a membrane-associated protein with calcium-channel activity, plays a key role in cartilage calcification during endochondral ossification. As a major constituent of cartilage matrix vesicles, which are released from microvilli of hypertrophic chondrocytes, it is involved in calcium uptake necessary for the initial stages of cartilage calcification. Little is known, however, concerning transcriptional regulation of the annexin A5 gene during chondrocyte differentiation. Here, we report on changes in annexin A5 expression by measuring mRNA and protein levels during in vitro differentiation of chick sternal chondrocytes to the hypertrophic phenotype. Terminal differentiation of mature sternal chondrocytes was achieved in the presence of sodium ascorbate in high-density cultures growing either in monolayer or over agarose as cell aggregates. Differentiation of chondrocytes to hypertrophic cells was followed by morphological analysis and by the onset of type X collagen expression. High expression levels of annexin A5 mRNA were detected in chondrocytes freshly isolated from the sterna by enzymatic digestion and subsequently in cells growing in monolayer, but annexin A5 gene transcription was rapidly downregulated when cells were grown in suspension as aggregates over agarose. However, protein levels did not decrease probably due to its low turnover rate. In suspension culture, annexin A5 mRNA reappeared after 3 weeks concomitantly with segregation of the aggregates into single cells and onset of chondrocyte hypertrophy. The downregulation of annexin A5 expression in cells growing as matrix-rich aggregates was reverted when extracellular matrix components were removed and cells were reseeded onto tissue culture plastic, suggesting that cell spreading, formation of focal contacts and stress fibers stimulated annexin A5 expression in proliferating as well as in hypertrophic chondrocytes.

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Mouse annexin V genomic organization includes an endogenous retrovirus

Cited by 8 publications

References 4 publications

Characterization of the Rodent Genes for Arylacetamide Deacetylase, a Putative Microsomal Lipase, and Evidence for Transcriptional Regulation

Characterization of the Rodent Genes for Arylacetamide Deacetylase, a Putative Microsomal Lipase, and Evidence for Transcriptional Regulation

Functional analysis of the human annexin A5 gene promoter: a downstream DNA element and an upstream long terminal repeat regulate transcription

Changes in the expression of annexin A5 gene during in vitro chondrocyte differentiation: Influence of cell attachment

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