Sequence analysis of the promoter regions of the classical class I gene RT1.A l and two other class I genes of the rat MHC

Lambracht, Doris; Wonigeit, K.

doi:10.1007/bf00163995

Cited by 21 publications

(7 citation statements)

References 17 publications

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“…The GenBank annotations of each find were then checked to determine which finds involved proposed TATA boxes. The genes identified by this search were rat GAP-43 (Nedivi et al, 1992), mouse major histocompatibility complex (M HC) Q10-K gene for class I antigen (Watts et al, 1989), mouse M HC Q2-k gene for class I antigen (Watts et al, 1989), mouse M HC D2d gene for class I antigen (Hedley et al, 1989), rat M HC RT1.A gene for class I antigen (Lambracht and Wonigeit, 1995), mouse proteasome L mp-7 (Z anelli et al, 1993), and chicken myelomonocytic growth factor (Sterneck et al, 1992). The synaptosomal-associated protein of 25 kDa (SNAP-25) and neuronal nitric oxide synthase (nNOS) sequences given in Figure 8 did not show up in this search, because their TATA boxes were not listed in the annotations for their GenBank entries.…”

Section: Methodsmentioning

confidence: 99%

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

Weber

Skene

1997

J. Neurosci.

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Multiple signaling pathways are thought to control the selective expression of genes over the course of neuronal differentiation. One approach to elucidating these pathways is to identify specific cis-acting elements that serve as the final targets for these signaling pathways in neural-specific genes. We now identify a novel repressive element from the growth-associated protein 43 (GAP-43) gene that can contribute to neuron-specific gene expression by inhibiting transcription in a wide range of non-neuronal cell types. This repressive element is located downstream of the GAP-43 TATA box and is highly positiondependent. When transferred to viral promoters this element preferentially inhibits transcription in non-neuronal cells. Electrophoretic mobility shift assays show that the repressive element comprises at least two protein recognition sites. One of these is a novel sequence motif that we designate the SNOG element, because it occurs downstream of the TATA boxes of the synaptosomal-associated protein of 25 kDa and neuronal nitric oxide synthase genes, as well as the GAP-43 gene. The GAP-43 repressive element is distinct in sequence and position dependence from the repressor element 1/neuron-restrictive silencer element previously described in other neural genes and therefore is a likely target for a distinct set of signaling pathways involved in the control of neuronal differentiation.

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Section: Methodsmentioning

confidence: 99%

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

Weber

Skene

1997

J. Neurosci.

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“…The promoter sequence for RT1-A l is from AF025309 [40], RT1-C l : AF025308 [40], H2-K b : M11847 [39], RT1-E2 n : AJ315490, RT1-E2 l : AJ537416. The comparison of the various boxed regulatory elements is discussed in the text.…”

Section: Resultsmentioning

confidence: 99%

“…Whereas H2-K b and RT1-A l contain a canonical TATA sequence, RT1-E2 shows the variant sequence TGTAA also found in RT1-C l and the mouse H2-Q6 to H2-Q9 genes (not shown here). Since MHC class I gene expression is also dynamically regulated by cytokines, we examined the three major elements within the upstream promoter region, namely the κB1 element [39,40], the Interferon Response Element (IRE) and site α, which is crucial for routes of activation involving the transcriptional coactivator CIITA [41,42]. All three sites were identified in the RT1-E2 promoters, but were found to diverge from those of other class I promoters by individual nucleotide differences that could presumably result in alterations of its activity.…”

Section: Resultsmentioning

confidence: 99%

Characterisation of RT1-E2, a multigenic family of highly conserved rat non-classical MHC class I molecules initially identified in cells from immunoprivileged sites

et al. 2003

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BackgroundSo-called "immunoprivileged sites" are tissues or organs where slow allograft rejection correlates with low levels of expression of MHC class I molecules. Whilst classical class I molecules are recognised by cytotoxic T lymphocytes (CTL), some MHC class I molecules are called "non-classical" because they exhibit low polymorphism and are not widely expressed. These last years, several studies have shown that these can play different, more specialised roles than their classical counterparts. In the course of efforts to characterise MHC class I expression in rat cells obtained from immunoprivileged sites such as the central nervous system or the placenta, a new family of non-classical MHC class I molecules, which we have named RT1-E2, has been uncovered.ResultsMembers of the RT1-E2 family are all highly homologous to one another, and the number of RT1-E2 loci varies from one to four per MHC haplotype among the six rat strains studied so far, with some loci predicted to give rise to soluble molecules. The RT1n MHC haplotype (found in BN rats) carries a single RT1-E2 locus, which lies in the RT1-C/E region of the MHC and displays the typical exon-intron organisation and promoter features seen in other rat MHC class I genes. We present evidence that: i) RT1-E2 molecules can be detected at the surface of transfected mouse L cells and simian COS-7 cells, albeit at low levels; ii) their transport to the cell surface is dependent on a functional TAP transporter. In L cells, their transport is also hindered by protease inhibitors, brefeldin A and monensin.ConclusionsThese findings suggest that RT1-E2 molecules probably associate with ligands of peptidic nature. The high homology between the RT1-E2 molecules isolated from divergent rat MHC haplotypes is particularly striking at the level of their extra-cellular portions. Compared to other class I molecules, this suggests that RT1-E2 molecules may associate with well defined sets of ligands. Several characteristics point to a certain similarity to the mouse H2-Qa2 and human HLA-G molecules.

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“…Four rat class I genes were located that contain significant sequence data 5Ј of the gene. One of these, RT 1.C, has been shown to be functional and does indeed contain the H-2 BF1 target sequence (32). Of the three remaining isolates, two are functional but are TLa-like (33,34), and the third is a pseudogene (35).…”

Section: Methodsmentioning

confidence: 99%

Activation Transcription Factor 1 Involvement in the Regulation of Murine H-2D Expression

Ishiguro

Brown

Meruelo

1997

Journal of Biological Chemistry

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Resistance to radiation leukemia virus-induced leukemia is correlated with an increase in H-2D expression on the thymocyte surface. Recently, it has been shown that elevated H-2D d expression on the infected thymocyte is a result of elevated mRNA transcription and that the transcriptional increase is correlated with elevated levels of a DNA binding activity, H-2 binding factor 1 (H-2 BF1), which recognizes the 5 -flanking sequences (5 -TGACGCG-3 ) of the H-2D d gene. This target for transcription factor binding has been found to be identical in the 5 -regulatory region of 12 rodent class I genes, nine of which have been shown to be functional genes. Furthermore, this cis-element is found 5 of 20 primate class I genes (15 human genes), seven of which are known to be functional. Here, we demonstrate that activation transcription factor 1 (ATF-1) is one component of H-2 BF1. In addition, the levels of ATF-1 mRNA in uninfected and radiation leukemia virus-infected thymocytes parallel those of H-2D d mRNA, and therefore, it is suggested that ATF-1 up-regulates the transcription of the H-2D d gene after radiation leukemia virus infection of thymocytes. Transfection experiments also demonstrate that ATF-1 activates a reporter plasmid that contains the H-2 BF1 motif, but not a reporter lacking this motif. This is the first demonstration of the interaction of ATF-1 with 5 -regulatory sequences of major histocompatibility complex class I genes.

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Sequence analysis of the promoter regions of the classical class I gene RT1.A l and two other class I genes of the rat MHC

Abstract: Sequence analysis of the promoter regions of the classical class I gene RT1.A and two other class I genes of the rat MHC

Cited by 21 publications

References 17 publications

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

Identification of a Novel Repressive Element That Contributes to Neuron-Specific Gene Expression

Characterisation of RT1-E2, a multigenic family of highly conserved rat non-classical MHC class I molecules initially identified in cells from immunoprivileged sites

Activation Transcription Factor 1 Involvement in the Regulation of Murine H-2D Expression

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