Expression Patterns In Brain Research Articles

Developmental expression of tenascin-C is altered by hypothyroidism in the rat brain

Tenascin-C is an extracellular matrix glycoprotein involved in cell adhesion and migration, and neurite outgrowth. Since these processes have been found to be under thyroid control in the developing rat brain, we have investigated the effect of congenital hypothyroidism on tenascin-C expression. At birth, in situ hybridization studies in hypothyroid rats show an abnormal up-regulation of tenascin-C in some areas (caudate–putamen, geniculate nuclei, ependymal epithelium of the lateral ventricles, hippocampus) and down-regulation in others (occipital and retrosplenial cortex, subiculum). With subsequent development, hypothyroid animals show higher tenascin-C expression also in the upper layers of the cerebral cortex and subplate, and the Bergmann glia of the cerebellum. Significantly, thyroxine treatment of hypothyroid rats led to normalization of tenascin-C levels in most areas. In agreement with the messenger RNA data, hypothyroid rats contain an uniformly higher level of immunoreactive tenascin-C protein throughout the brain, particularly in the cerebellum. Suggesting a direct cellular effect, thyroid hormone also decreases tenascin-C expression in two glial cell lines (C6, B3.1) expressing thyroid receptors. Our results show that congenital hypothyroidism causes specific alterations in the pattern of tenascin-C expression in the rat brain which may at least partially be responsible for some of the developmental disturbances observed in this syndrome.

Time course and localization patterns of interleukin-1β messenger rna expression in brain and pituitary after peripheral administration of lipopolysaccharide

The inflammatory cytokine interleukin-1 has been implicated as a mediator of many centrally controlled responses, such as fever and increased activity of the hypothalamic-pituitary-adrenal axis, after systemic infections. To identify the neuroanatomical loci of brain interleukin-l-producing cells during infection, we investigated interleukin-1β messenger RNA expression by in situ hybridization histochemistry using a 500 nt ribonucleotide probe applied on brain sections from rats injected intraperitoneally with 2.5 mg/kg bacterial lipopolysaccharide or saline. In control animals, interleukin-1β messenger RNA was not detectable. In the brains of lipopolysaccharide-injected animals, two temporally and spatially distinct waves of interleukin-1β messenger RNA induction were observed. First, cell labelling appeared at 0.5 h, peaked at 2 h, and declined at 4–8 h. The labelled cells were concentrated in circumventricular organs - organum vasculosum of the lamina terminalis, subfornical organ, median eminence and area postrema - and in choroid plexus, meninges, and blood vessels. Second, at 8–12 h, scattered small cells became labelled throughout the entire brain parenchyma; the labelling subsided by 24 h. Labelling was not observed in any neurons. In the pituitary, lipopolysaccharide induced strong interleukin-1(3 messenger RNA expression initially in the anterior lobe at 0.5-1 h, and later in the neural lobe at 1–2 h, and subsiding thereafter. The results show that at early time points, peripheral lipopolysaccharide induces interleukin-1β message production at the blood brain barrier and in circumventricular organs where the blood-brain barrier is leaky. After a time delay of 6–10 h, however, interleukin-1β messenger RNA is primarily expressed by non-neuronal cells of the brain in the brain parenchyma. These results suggest that the source of initial brain IL-1 activity after peripheral lipopolysaccharide injection derives from cells of the blood-brain barrier and the circumventricular organs, and the sustained interleukin-1 activity in the central nervous system thereafter is derived from glia.

Modulation of Igf2 genomic imprinting in mice induced by 5-azacytidine, an inhibitor of DNA methylation.

The adjacent genes, insulin-like growth factor 2 (Igf2) and H19, are imprinted in both mouse and human. While Igf2 is expressed from the paternal allele, H19 is transcribed exclusively from the maternal allele. To explore the underlying mechanism of Igf2 and H19 imprinting, we studied the effect of DNA demethylation on allelic expression by injecting mice with the demethylating agent 5-azacytidine (5-aza-C). We observed a > or = 2-fold increase in the abundance of Igf2 mRNA in liver from treated mice compared with that of control mice. There was no significant change in Igf2 or H19 expression in brain. In the 5-aza-C-treated mice, there was dramatic modulation of Igf2 imprinting. In some tissues, Igf2 was expressed biallelically, while in other tissues, the paternal allele was silenced and the normally imprinted maternal allele was expressed, an example of allelic switching. There was no change in the normal biallelic pattern of Igf2 expression in brain. H19, on the other hand, remained imprinted in all tissues in mice treated with 5-aza-C. These results provide the first example of a pharmacological manipulation of genomic imprinting of an endogenous gene in vivo and further implicate DNA methylation as an important factor in maintaining the differential allelic expression of the Igf2 gene.

Complex regulatory region mediating tailless expression in early embryonic patterning and brain development.

tailless encodes a transcription factor expressed in multiple domains in the developing embryo. Early and transient expression at the posterior pole is required to establish a domain from which the eighth abdominal segment, telson and posterior gut arise. Just a few nuclear cycles later, a brain-specific domain is initiated at the anterior; expression in this domain is maintained with complex modulations throughout embryogenesis. Expression of tailless in this domain is required to establish the most anterior region of the brain. To understand the function and regulation of these different domains of expression, we provide a detailed description of tailless expression in brain neuroblasts and show that this expression is not detectably regulated by the head gap genes buttonhead or orthodenticle, by the proneural gene lethal of scute or by tailless itself. We show that approximately 6 kb of sequenced upstream regulatory DNA can drive lacZ expression in a pattern that mimics the full tailless embryonic expression pattern. Within this sequence we identify multiple modules responsible for different aspects of the tailless pattern. In addition to identifying additional torso response elements that mediate early blastoderm polar expression, we show that the complex brain expression pattern is driven by a combination of modules; thus expression at a low level throughout the brain and at a high level in the dorsal medial portion of the brain and in the optic lobe, as well as neuroblast-specific repression are mediated by different DNA regions.

Regulators of G-Protein Signaling (RGS) Proteins: Region-Specific Expression of Nine Subtypes in Rat Brain

The recently discovered regulators of G-protein signaling (RGS) proteins potently modulate the functioning of heterotrimeric G-proteins by stimulating the GTPase activity of G-protein alpha subunits. The mRNAs for numerous subtypes of putative RGS proteins have been identified in mammalian tissues, but little is known about their expression in brain. We performed a systematic survey of the localization of mRNAs encoding nine of these RGSs, RGS3-RGS11, in brain by in situ hybridization. Striking region-specific patterns of expression were observed. Five subtypes, RGS4, RGS7, RGS8, RGS9, and RGS10 mRNAs, are densely expressed in brain, whereas the other subtypes (RGS3, RGS5, RGS6, and RGS11) are expressed at lower density and in more restricted regions. RGS4 mRNA is notable for its dense expression in neocortex, piriform cortex, caudoputamen, and ventrobasal thalamus. RGS8 mRNA is highly expressed in the cerebellar Purkinje cell layer as well as in several midbrain nuclei. RGS9 mRNA is remarkable for its nearly exclusive enrichment in striatal regions. RGS10 mRNA is densely expressed in dentate gyrus granule cells, superficial layers of neocortex, and dorsal raphe. To assess whether the expression of RGS mRNAs can be regulated, we examined the effect of an acute seizure on levels of RGS7, RGS8, and RGS10 mRNAs in hippocampus. Of the three subtypes, changes in RGS10 levels were most pronounced, decreasing by approximately 40% in a time-dependent manner in response to a single seizure. These results, which document highly specific patterns of RGS mRNA expression in brain and their ability to be regulated in a dynamic manner, support the view that RGS proteins may play an important role in determining the intensity and specificity of signaling pathways in brain as well as their adaptations to synaptic activity.

The regional pattern of D4 gene expression in human brain

Using a competitive reverse transcription-polymerase chain reaction (RT-PCR) assay levels of D4 gene expression have been determined in 16 regions obtained from a single control brain. Relatively high levels of expression were detected in the prefrontal and temporolimbic structures whilst low levels were detected in striatal regions. This pattern correlates with the reported distribution of the D4 receptor.

TGT3, Thyroid Transcription Factor I, and Sp1 Elements Regulate Transcriptional Activity of the 1.3-Kilobase Pair Promoter ofT1α, a Lung Alveolar Type I Cell Gene

Alveolar type I epithelial cells form the major surface for gas exchange in the lung. To explore how type I cells differ in gene expression from their progenitor alveolar type II cells, we analyzed transcriptional regulation of T1alpha, a gene expressed by adult type I but not type II cells. In vivo developmental patterns of T1alpha expression in lung and brain suggest active gene regulation. We cloned and sequenced 1.25 kilobase pairs of the T1alpha promoter that can drive reporter expression in lung epithelial cell lines. Deletion analyses identified regions important for lung cell expression. The base pair (bp) -100 to -170 fragment conferred differential regulation in lung epithelial cells compared with fibroblasts. Sequence alignment of this fragment with type II-specific surfactant protein B and C promoters shows similar consensus elements arranged in a different order. Gel retardation studies with alveolar epithelial cell line nuclear extracts, thyroid transcription factor I (TTF-1) homeodomain, hepatic nuclear factor (HNF)-3beta, or Sp1 proteins, and supershift assays were used to characterize TTF-1, HNF-3 (TGT3), and Sp1/Sp3 binding sites. The TGT3 site binds factors with binding properties similar to HNF-3/Fkh (hepatic nuclear factor-3/forkhead) proteins but different from HNF-3alpha or HNF-3beta. Co-transfection with a TTF-1 expression vector moderately transactivated the -170 bp-reporter construct. Mutational analysis of these three binding sites showed reduced transcriptional activity of the -170 bp promoter. Therefore, several regulatory sequences involved in type II cell gene regulation are also present in the T1alpha promoter, suggesting that genes of the peripheral lung epithelium may be regulated by similar factors.

Cholecystokinin A and B receptors are differentially expressed in normal pancreas and pancreatic adenocarcinoma.

Cholecystokinin (CCK) plays an important role in pancreatic carcinogenesis. While human CCK-A and -B receptors have been fully characterized, their relative roles in human pancreatic adenocarcinoma remain unclear. Thus, expression of CCK-A and -B receptors in normal human pancreas, pancreatic adenocarcinomas, and other human extrapancreatic tissues and malignancies was examined, using reverse transcription followed by the polymerase chain reaction (RT-PCR). mRNA isolated from 15 normal pancreas specimens, 22 pancreatic adenocarcinomas, and 58 extrapancreatic tissues and tumors was subjected to RT-PCR using primers specific for human CCK-A and -B receptors. Expression of CCK-B receptors was detected in all tissues arising from pancreas and in most extrapancreatic tissues and tumors. In contrast, CCK-A receptors exhibited a more selective pattern of expression in gall bladder, intestine, brain, ovary, spleen, and thymus. Of significance, CCK-A receptors were expressed selectively in all pancreatic adenocarcinomas, but not in any normal pancreas specimens. In situ hybridization, using receptor-specific riboprobes, localized CCK-A receptor expression to ductal cells, the presumed origin of most human pancreatic adenocarcinomas. Southern blot analysis revealed no evidence of CCK-A receptor gene amplification or rearrangement in pancreatic adenocarcinomas. Because of its selective expression, the CCK-A receptor may serve as selective biomarker for pancreatic adenocarcinoma.

Neuregulin-2, a new ligand of ErbB3/ErbB4-receptor tyrosine kinases.

The neuregulins (NRGs) are a family of multipotent epidermal-growth-factor-like (EGF-like) factors that arise from splice variants of a single gene. They influence the growth, differentiation, survival and fate of several cell types. We have now discovered a set of new neuregulin-like growth factors, which we call neuregulin-2 (NRG-2): these are encoded by their own gene and exhibit a distinct expression pattern in adult brain and developing heart. Like NRG-1, the EGF-like domain of the new ligands binds to both the ErbB3- and ErbB4-receptor tyrosine kinases. However, NRG-2 stimulates different ErbB-receptor tyrosine-phosphorylation profiles from NRG-1. Our results indicate that NRG-1 and NRG-2 mediate distinct biological processes by acting at different sites in tissues and eliciting different biochemical responses in cells.

Differential expression of FMR1, FXR1 and FXR2 proteins in human brain and testis.

Lack of expression of the fragile X mental retardation protein (FMRP) results in mental retardation and macroorchidism, seen as the major pathological symptoms in fragile X patients. FMRP is a cytoplasmic RNA-binding protein which cosediments with the 60S ribosomal subunit. Recently, two proteins homologous to FMRP were discovered: FXR1 and FXR2. These novel proteins interact with FMRP and with each other and they are also associated with the 60S ribosomal subunit. Here, we studied the expression pattern of the three proteins in brain and testis by immunohistochemistry. In adult brain, FMR1, FXR1 and FXR2 proteins are coexpressed in the cytoplasm of specific differentiated neurons only. However, we observed a different expression pattern in fetal brain as well as in adult and fetal testis, suggesting independent functions for the three proteins in those tissues during embryonic development and adult life.

Brain substrates activated by electroacupuncture of different frequencies (I): comparative study on the expression of oncogene c- fos and genes coding for three opioid peptides

Low and high frequency electroacupuncture (EA)-produced analgesia have been shown to be mediated by different brain substrates and different opioid peptides. In this study, Fos-like immunoreactivity (FLI) and in situ hybridization of the three opioid mRNAs were used to examine the effect of low (2 Hz) and high (100 Hz) frequency EA on neuronal activities and the expression of opioid genes. 2 Hz and 100 Hz EA induced a markedly different spatial patterns of Fos expression in the rat brain, suggesting there are distinct neuronal pathways underlying EA of different frequencies. Likewise, 2 Hz and 100 Hz EA exert differential effects on opioid gene expression: while 2 Hz EA induced a more extensive and intensive preproenkephalin (PPE) mRNA expression than 100 Hz EA, it had no effect on preprodynorphin (PPD) mRNA expression which was significantly increased by 100 Hz EA stimulation. In contrast, EA of both frequencies did not affect POMC mRNA expression.

Valentino: a zebrafish gene required for normal hindbrain segmentation.

Mutational analysis can serve both to identify new genes essential for patterning embryonic development and to determine their functions. Here we describe the identification and phenotypic characterization of alleles of valentino, which we recovered in a genetic screen that sought to identify mutations in the zebrafish that disrupt region-specific gene expression patterns in the embryonic brain. valentino is required for normal hindbrain segmentation and the hindbrain of valentino mutant embryos is shortened by the length of one rhombomere. We demonstrate that valentino is required cell-autonomously in the development of rhombomeres 5 and 6, and propose that valentino functions in the subdivision and expansion of a common precursor region in the presumptive hindbrain into the definitive rhombomeres 5 and 6. These results provide genetic evidence for a two-segment periodicity in the hindbrain and suggest that this periodicity arises sequentially, through the specification and later subdivision of a two-rhombomere unit, or 'protosegment'.

Temporal-spatial pattern of c-Fos expression in the rat brain in response to indispensable amino acid deficiency. II. The learned taste aversion.

Rats rapidly become anorectic when eating an amino acid-imbalanced diet that induces a deficiency of an indispensable amino acid. Recognition of amino acid deficiency is thought to be a function of the anterior piriform cortex. However, the neuronal circuitry underlying the secondary learned aversion to such diets may involve the amygdala. In this study, Fos immunohistochemistry was employed to identify regions of the brain activated during the learned aversion phase of the response to an amino acid-imbalanced diet. c-Fos expression was examined in the brains of rats at intervals from 1 to 6 h after introduction of a diet imbalanced in threonine, a corrected (amino acid-balanced) diet or a basal (low protein) diet. The study has revealed that, within the time frame associated with the learned aversive response, Fos-immunoreactive (Fos-IR) neurons increased selectively in the central nucleus of the amygdala in animals fed a threonine-imbalanced diet. These results suggest a temporal relationship between changes in neuronal activity in the central nucleus of the amygdala and the learned aversion associated with acute amino acid deficiency.

Temporal-spatial pattern of c-fos expression in the rat brain in response to indispensable amino acid deficiency. I. The initial recognition phase.

Rats reduce their food intake after ingestion of a small amount of an amino acid imbalanced (AA-IMB) diet that induces a pronounced amino acid deficiency. Two hours after ingesting a threonine-IMB diet, just when food intake is depressed significantly, the concentration of threonine is decreased in some but not all brain areas. Neural recognition of this decrease in the limiting amino acid is thought to be the first step in the anorectic responses to AA-IMB diets. To identify the regions of the brain that may be activated upon recognition of an AA-IMB diet, we examined the temporal-spatial distribution of Fos immunoreactive neurons at intervals after introduction of either threonine-IMB or control diets. We found that Fos immunoreactivity in the anterior piriform cortex and immediately surrounding areas, along with the infralimbic cortex, was increased selectively early (by 2 h) after introduction of the AA-IMB diet, and remained elevated through 3 h. The anterior piriform cortex is believed to function in neural recognition of amino acid deficiency. Fos immunoreactivity in the AA-IMB group increased over the control diet groups somewhat later in the dorsomedial nucleus of the hypothalamus. We hypothesize that these areas in the rostral forebrain may serve as neural relays in the early phases of the anorectic responses that occur upon recognition of amino acid deficiency.

Temporal-spatial pattern of c-fos expression in the rat brain in response to indispensable amino acid deficiency I. The initial recognition phase

Rats reduce their food intake after ingestion of a small amount of an amino acid imbalanced (AA-IMB) diet that induces a pronounced amino acid deficiency. Two hours after ingesting a threonine-IMB diet, just when food intake is depressed significantly, the concentration of threonine is decreased in some but not all brain areas. Neural recognition of this decrease in the limiting amino acid is thought to be the first step in the anorectic responses to AA-IMB diets. To identify the regions of the brain that may be activated upon recognition of an AA-IMB diet, we examined the temporal-spatial distribution of Fos immunoreactive neurons at intervals after introduction of either threonine-IMB or control diets. We found that Fos immunoreactivity in the anterior piriform cortex and immediately surrounding areas, along with the infralimbic cortex, was increased selectively early (by 2 h) after introduction of the AA-IMB diet, and remained elevated through 3 h. The anterior piriform cortex is believed to function in neural recognition of amino acid deficiency. Fos immunoreactivity in the AA-IMB group increased over the control diet groups somewhat later in the dorsomedial nucleus of the hypothalamus. We hypothesize that these areas in the rostral forebrain may serve as neural relays in the early phases of the anorectic responses that occur upon recognition of amino acid deficiency.

Expression of brain-type creatine kinase and ubiquitous mitochondrial creatine kinase in the fetal rat brain: evidence for a nuclear energy shuttle.

To test the hypothesis that embryonic brain cells utilize a creatine phosphate energy shuttle, we examined the pattern of creatine kinase (CK) isoform expression and localization in the fetal rat brain. Moderate levels of CK activity are present at embryonic day 14 (7 U/mg protein) and decrease slightly until 3 days postpartum followed by a rapid, fourfold up-regulation to adult levels by 1 month (18 U/mg protein). In parallel with changes in enzyme activity, there is a biphasic and coordinate pattern of expression of brain-type CK (BCK) and ubiquitous mitochondrial CK (uMtCK) determined by nondenaturing electrophoresis and immunoblot analysis. The localization of CK isoforms was examined by immunocytochemistry, and, during the fetal period, BCK and uMtCK immunoreactivity was detected throughout the central and peripheral nervous system, especially in neuroepithelial regions of the cerebral vesicles and spinal cord. In large cells within the olfactory neuroepithelium and ventral spinal cord, differential compartmentation of CK isoforms was evident, with BCK localized primarily in cell nuclei, whereas uMtCK immunoreactivity was present in the cell body (but not within nuclei). In olfactory bulb neuroepithelium, both isoforms were expressed in the middle zone of the germinal layer associated with DNA synthesis. In embryonic skeletal and cardiac muscle, which also express BCK, the same compartmentation of BCK was seen, with BCK localized primarily in the cell nucleus of cardiac and skeletal myoblasts. These results demonstrate a coordinate pattern of expression and compartmentation of BCK and uMtCK isoforms in the fetal brain that, in some cells, provides the anatomic basis for a nuclear energy shuttle.

Developmental pattern of GFAP and vimentin gene expression in rat brain and in radial glial cultures

In the present study we analyze the events which occur during the early stages of astrogliogenesis by examining the pattern of both GFAP and vimentin gene expression and their corresponding immunoreactive proteins during rat brain development. This study was carried out "in vivo" (whole brain) and "in vitro" (primary culture of radial glia) using immunofluorescence, immunoblotting, and Northern blot analysis. Our results demonstrate that although GFAP immunostaining appeared late in gestation and at day 5 in radial glia cultures, GFAP mRNA expression was first detected, at very low levels, on fetal (F) day 15 and increased to F21. During postnatal development a striking increase in GFAP and its encoding messenger occurs. In contrast, the levels of vimentin and its mRNA expression were very high during the fetal stage (F15 to F21). Thereafter vimentin expression declined during postnatal (P) development until P21 and then remained constant at adult levels. In contrast, an increase in vimentin expression was observed in glial cells throughout the entire culture period. The biological significance of the developmental patterns of GFAP and vimentin expression in astroglial cells. during brain development is discussed.

GapIII, a new brain-enriched member of the GTPase-activating protein family.

Ras GTPase-activating proteins (GAPs) are negative regulators of ras, which controls proliferation and differentiation in many cells. Ras GAPs have been found in a variety of species from yeast to mammals. We describe here a newly identified mammalian GAP, GapIII, which was obtained by differential screening of a rat oligodendrocyte cDNA library. GapIII putatively encodes a 834 amino acid protein with a predicted molecular weight of 96 kDa, which contains a consensus GAP-related domain (GRD). The protein encoded by this cDNA has high homology with Gap1m, which was recently identified as a putative mammalian homolog of Drosophila Gap1. These proteins contain three structural domains, an N-terminal calcium-dependent phospholipid binding domain, GRD, and a C-terminal PH/Btk domain. Because of the sequence homology and the structural similarities of this protein with Gap1m, we hypothesize that GapIII and Gap1m may be members of a mammalian GAP gene family, separate from p120GAP, neurofibromin (NF1), and IQGAP. To confirm the GapIII protein activity, constructs containing different GapIII-GRD domains were transformed into iral mutant yeast to determine their relative ability to replace IRA1 functionally. Constructs that contained essentially the full-length protein (all three domains), the GRD alone, or the GRD plus PH/Btk domain suppressed heat shock sensitivity of ira1, whereas constructs that contained the GRD with part of the PH/Btk domain had only a weak ability to suppress heat shock sensitivity. These results suggest that the GapIII GRD itself is sufficient to down-regulate ras proteins in yeast. Expression of GapIII mRNA (4.2 kb) was examined by Northern analysis and in situ hybridization. This mRNA was expressed at highest levels in the brain, where its expression increased with development. Lower levels of the mRNA were expressed in the spleen and lung. Among neural cells, GapIII mRNA was expressed in neurons and oligodendrocytes, but not in astrocytes. Interestingly, the expression pattern in brain is reminiscent of type 1 NF1 expression reported by Gutmann et al. (Cell Growth Differ in press, 1995). We propose that in addition to p120GAP and neurofibromin, the GapIII/Gap1m family may be important for modulating ras activity in neurons and oligodendrocytes during normal brain development and in particular in the adult brain.

Regional expression and cellular localization of the Na(+)-dependent inorganic phosphate cotransporter of rat brain

We have recently isolated and identified a brain specific Na(+)-dependent inorganic phosphate (Pi) cotransporter cDNA (rBNPI) from a rat brain cDNA library (Ni, et al., 1994). We now report the regional and developmental expression, as well as the cellular localization, of rBNPI mRNA in the rat brain. In situ hybridization histochemistry reveals that rBNPI mRNA is selectively expressed in neuron-enriched regions of the adult rat brain, such as the cerebral cortex, hippocampus, and cerebellum. Cellular localization of rBNPI transcripts reveals expression in both pyramidal and granule neurons in these regions. By contrast, little to no hybridization signal was observed in white matter-enriched areas such as the corpus callosum. The expression of rBNPI mRNA was determined during pre- and postnatal development of the rat CNS. From embryonic day 17 to early postnatal day 10 (PND 10), there is a rather widespread but diffuse pattern of rBNPI expression in brain. During late postnatal development, however, the expression of rBNPI mRNA becomes confined to discrete populations of neurons in the cerebral cortex, hippocampus, and cerebellum. Thus, rBNPI expression is developmentally regulated and abundant levels of mRNA are found in rather discrete populations of neurons in the adult rat brain. The latter suggests that rBNPI may serve to selectively regulate intracellular Pi transport in certain neurons for either metabolic and (or) signaling events.

The embryonic RNA helicase gene (ERH): a new member of the DEAD box family of RNA helicases.

DEAD box proteins share several highly conserved motifs including the characteristic Asp-Glu-Ala-Asp (D-E-A-D in the amino acid single-letter code) motif and have established or putative ATP-dependent RNA helicase activity. These proteins are implicated in a range of cellular processes that involve regulation of RNA function, including translation initiation, RNA splicing and ribosome assembly. Here we describe the isolation and characterization of an embryonic RNA helicase gene, ERH, which maps to mouse chromosome 1 and encodes a new member of the DEAD box family of proteins. The predicted ERH protein shows high sequence similarity to the testes-specific mouse PL10 and to the maternally acting Xenopus An3 helicase proteins. The ERH expression profile is similar, to that of An3, which localizes to the animal hemisphere of oocytes and is abundantly expressed in the embryo. ERH is expressed in oocytes and is a ubiquitous mRNA in the 9 days-post-conception embryo, and at later stages of development shows a more restricted pattern of expression in brain and kidney. The similarities in sequence and in expression profile suggest that ERH is the murine equivalent of the Xenopus An3 gene, and we propose that ERH plays a role in translational activation of mRNA in the oocyte and early embryo.