Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ectopic”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed1997

Suppression of matrix metalloproteinases inhibits establishment of ectopic lesions by human endometrium in nude mice.

Matrix metalloproteinases of the stromelysin family are expressed in the human endometrium as a consequence of cellular events during the menstrual cycle that require extracellular matrix remodeling. We have recently documented the presence of these enzymes in lesions of endometriosis, a benign disease that presents as persistent ectopic sites of endometrial tissue, usually within the peritoneal cavity. Endometriosis can develop after retrograde menstruation of endometrial tissue fragments, and establishment of ectopic sites within the peritoneal cavity requires breakdown of extracellular matrix. To examine whether matrix metalloproteinases might contribute to the steroid-dependent epidemiology and cellular pathophysiology of endometriosis, we have developed an experimental model of endometriosis using athymic nude mice as recipients of human endometrial tissue. Our results demonstrate that estrogen treatment of human endometrial tissue in organ culture maintains secretion of matrix metalloproteinases, and promotes establishment of ectopic peritoneal lesions when injected into recipient animals. In contrast, suppressing metalloproteinase secretion in vitro with progesterone treatment, or blocking enzyme activity with a natural inhibitor of metalloproteinases, inhibits the formation of ectopic lesions in this experimental model.

Adult↗
PubMed2006

Ectopic pancreas formation in Hes1 -knockout mice reveals plasticity of endodermal progenitors of the gut, bile duct, and pancreas.

Ectopic pancreas is a developmental anomaly occasionally found in humans. Hes1, a main effector of Notch signaling, regulates the fate and differentiation of many cell types during development. To gain insights into the role of the Notch pathway in pancreatic fate determination, we combined the use of Hes1-knockout mice and lineage tracing employing the Cre/loxP system to specifically mark pancreatic precursor cells and their progeny in Ptf1a-cre and Rosa26 reporter mice. We show that inactivation of Hes1 induces misexpression of Ptf1a in discrete regions of the primitive stomach and duodenum and throughout the common bile duct. All ectopic Ptf1a-expressing cells were reprogrammed, or transcommitted, to multipotent pancreatic progenitor status and subsequently differentiated into mature pancreatic exocrine, endocrine, and duct cells. This process recapitulated normal pancreatogenesis in terms of morphological and genetic features. Furthermore, analysis of Hes1/Ptf1a double mutants revealed that ectopic Ptf1a-cre lineage-labeled cells adopted the fate of region-appropriate gut epithelium or endocrine cells similarly to Ptf1a-inactivated cells in the native pancreatic buds. Our data demonstrate that the Hes1-mediated Notch pathway is required for region-appropriate specification of pancreas in the developing foregut endoderm through regulation of Ptf1a expression, providing novel insight into the pathogenesis of ectopic pancreas development in a mouse model.

Animals↗
PubMed2000

Ventricular ectopic activity, left ventricular mass, hyperinsulinemia, and intracellular magnesium in normotensive patients with obesity.

Insulin resistance, a well-known feature of obesity, is associated with several pathological changes, which are potentially arrhythmogenic. Ventricular ectopic activity in normotensive obese patients has not been studied in detail. Therefore the authors designed a study to investigate potential relationships among ventricular ectopic activity, left ventricular mass, hyperinsulinemia, and intracellular magnesium concentration in obese patients. Thirty-two obese patients and 32 nonobese control subjects, who were referred to outpatient department because of ventricular ectopy, participated in the study. The groups were matched for age and gender. All had normal glucose tolerance. All subjects underwent a 75-g glucose tolerance test, and blood samples were obtained at 30, 60, and 120 minutes thereafter for determination of glucose and insulin concentrations. Echocardiography was performed and left ventricular mass index was calculated. The number of ventricular ectopic beats per hour (VEB/hour) was recorded by 24-hour ECG Holter monitoring. Plasma and erythrocyte magnesium concentrations were determined by atomic absorption spectrophotometer. Obese patients had higher body weight, body mass index, heart rate, and left ventricular mass index. Obese subjects had higher fasting insulin as well as insulin/glucose ratio and broader area under the curve of insulin (AUC-I) compared to nonobese subjects. Insulin sensitivity appeared to be lower in the obese group. Holter monitoring showed more VEB/hour in the obese group. Magnesium concentration in serum and in erythrocytes was lower in obese persons. In the obese group a positive correlation was found between left ventricular mass index and fasting insulin (r=0.345, p=0.027), insulin/glucose index (r=0.351, p=0.049), and AUC-I (r=0.405, p=0.011). The number of VEB/hour in obese patients was in positive correlation with age (r=0.681, p<0.001), left ventricular mass index (r=0.542, p=0.001), fasting insulin (r=0.380, p=0.016), and AUC-I (r=0.493, p=0.002) and in negative correlation with magnesium concentration in erythrocytes (r=-0.457, p=0.004). Multiple regression analysis showed that age and AUC-I are the only determinants of VEB/hour and together explained 56% of the variability in the obese subjects. It appears that in obese normotensive subjects, ventricular ectopic beats are related to age, insulin resistance, left ventricular mass index, and decreased intracellular magnesium content.

Aged↗
PubMed1984

Technetium pertechnetate scintigraphy to detect ectopic gastric mucosa in Meckel's diverticulum.

Tc-pertechnetate scintigraphy was performed in 81 infants and children, clinically suspected to have Meckel's diverticulum with ectopic gastric mucosa. The predominant symptom was rectal bleeding and anemia. Twenty-two patients underwent laparotomy and 12 had Meckel's diverticulum with ectopic gastric mucosa. In operated patients the sensitivity of scintigraphy in detecting ectopic gastric mucosa was 0.75, the specificity 1.0 and the diagnostic accuracy 0.86; the diagnostic accuracy was estimated to 0.96 for the whole material. Histologic examination of the diverticula showed a smaller area of the ectopic mucosa in cases with negative scintigraphic findings. In addition, prominent fibrosis seemed to be a more consistent finding in cases with negative as opposed to those with positive scintigraphic findings. Presence of anemia may provide a guideline as to whether or not scintigraphy is indicated.

Adolescent↗
PubMed2006

Ectopic cartilage formation induced by mesenchymal stem cells on porous gelatin-chondroitin-hyaluronate scaffold containing microspheres loaded with TGF-beta1.

The study aimed to produce a novel porous gelatin-chondroitin-hyaluronate scaffold in combination with a controlled release of TGF- beta1 and to evaluate its potentials in ectopic cartilage formation. The gelatin-chondroitin-hyaluronate scaffold was developed to mimic the natural extra cellular matrix of cartilage. Gelatin microspheres loaded with TGF- beta1 (MS-TGF beta1) showed a fast cytokine release at initial phase (37.4%) and the ultimate accumulated release was 83.1% by day 18. Then MS-TGF beta1 were incorporated into scaffold. The MSCs seeded on scaffold with or without MS-TGF beta1 were incubated in vitro or implanted subcutaneously in nude mice. In vitro study showed that, compared to the scaffold, the scaffold/MS-TGF beta1 significantly augmented the proliferation of MSCs and GAG synthesis. Three weeks postoperatively histology observation showed that in MSCs/scaffold/MS-TGF beta1 implantation group, cells of newly formed ectopic cartilage were located within typical lacunae and demonstrated morphological characteristics of chondrocytes. Six weeks later the ectopic cartilage grew more and islands of cartilage were observed. The matrix was extensively metachromatic by safranin-O/Fast green staining. Immunohistochemical staining also indicated ectopic cartilage was intensely stained for type II collagen. Instead, in the MSCs/scaffold implantation group, no cartilage-like tissue formed and matrix showed negative or weak positive staining. The percentage of positive staining area was significantly larger in MSCs/scaffold/MS-TGF beta1 group (p<0.05) at each time point. The results indicated that the novel gelatin-chondroitin-hyaluronate scaffold with MS-TGF beta1 could induce the chondral differentiation of MSCs to form cartilage and might serve as a new way to repair cartilage defects.

Animals↗
PubMed2006

Ectopic thyroid in an adrenal mass: a case report.

BACKGROUND: It is difficult to explain ectopic thyroid beneath the diaphragm because during the development the thyroid descends from the tongue to the anterior of the trachea. A few cases of ectopic lesions have been reported in the literature for abdominal organs including the adrenal glands, but the mechanism by which the thyroid components migrate into the abdomen has been poorly understood. CASE PRESENTATION: A 54-year-old woman was diagnosed as having an adrenal mass. Laparoscopic adrenalectomy was carried out. Microscopically, the mass was composed of normal adrenal and ectopic thyroid tissues. CONCLUSION: We herein describe the fourth case reported of ectopic thyroid in the adrenal gland.

Adrenal Gland Diseases↗
PubMed2004

Ubiquitin is associated with the survival of ectopic stromal cells in endometriosis.

BACKGROUND: Endometriosis is a condition that affects women of reproductive age, where the glandular and/or stromal tissues from the eutopic endometrium implant in ectopic locations. It is well established that the survival of ectopic implants is due to lower levels of apoptosis, but no consensus exists as to which pathway/s this is mediated by. The ubiquitin protein shares a similar sequence homology to an anti-apoptotic protein called BAG-1 and is expressed in the normal endometrium. Currently, no studies have been conducted to determine ubiquitin expression and its possible anti-apoptotic effects in endometriosis. METHODS: Archived endometrial tissues from endometriosis patients and women undergoing laparoscopic diagnosis (controls) from January 2000 to July 2003 at Westmead Hospital were examined, where 14 cases of endometriosis and 55 controls were included in the study. RESULTS: Both the ubiquitin protein and apoptosis were expressed in both glandular and stromal cells throughout the menstrual cycle of the eutopic endometrium, in which ubiquitin exhibited a cyclic expression, reaching a peak in late proliferative phase. In contrast, ubiquitin was predominantly expressed in cells of stromal origin in endometriosis, was no longer regulated by a cyclic pattern and was associated with an aberrant level of cell survival. CONCLUSIONS: For the first time, this study shows that ubiquitin is expressed in endometriotic cells and may contribute to a reduced sensitivity of ectopic endometrial tissue to apoptosis. These findings also suggest that stromal cells contribute differentially to the development of ectopic endometrial tissue.

Adult↗
PubMed1981

Use of glycosidase digested human chorionic gonadotropin beta-subunit to explain the partial binding of ectopic glycoprotein hormones to Con A.

Recent studies have demonstrated that ectopic glycoprotein hormones only partially bind Con A. To investigate the basis for these findings, the Con A binding of ectopic hCG beta from DoT cervical carcinoma cells was examined after digestion with various glycosidases. Ectopic hCG beta only partially bound Con A, as was the case after digestion with neuraminidase and beta-galactosidase. However, subsequent digestion with N-acetylhexosaminidase increased Con A binding to 96%. It is apparent that Con A binding of ectopic hCG can be inhibited by a residue removed by N-acetylhexosaminidase, probably extra beta-N-acetylglucosamine linked to beta-mannose on N-linked oligosaccharides. The method used involved the glycosidase digestion of glycoprotein alkylated under denaturing conditions and was first validated with milligram amounts of standard hCG beta.

Acetylglucosaminidase↗
PubMed1987

Ectopic beta-human chorionic gonadotropin production by a human hepatoma cell line (FOCUS): isolation and immunochemical characterization.

We have established a human hepatocellular carcinoma cell line designed FOCUS that produces and secretes the beta-subunit of hCG. In the study of beta hCG production by FOCUS cells, we have developed and employed a series of monoclonal immunoradiometric assays (IRMAs) that detect epitopes unique to beta hCG, alpha hCG, hCG, and sequence-specific regions of the carboxyl-terminal peptide of beta hCG. The cells secrete approximately 15 ng beta hCG/10(6) cells and per 24 h; however, we were unable to detect either hCG or the alpha-subunit. The ectopic beta hCG was subsequently affinity purified from the culture medium and partially characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. The mol wt of ectopic beta hCG was approximately 35,000 daltons. Immunochemical analysis of ectopic beta hCG by sequence-specific monoclonal antibodies revealed that epitopes corresponding to amino acid sequences 109-115, 121-145, 134-140, and 139-145 of the carboxyl-terminal peptide were present. FOCUS cells also demonstrate an intracytoplasmic localization of beta hCG by immunoperoxidase-staining techniques. Taken together, these findings suggest that FOCUS cells produce and secrete only beta hCG and that thus far, its physical properties appear indistinguishable from those of the native subunit. This unique cell line will be useful to study beta hCG gene(s) regulation as well as the mechanisms of ectopic beta hCG production and secretion.

Antibodies, Monoclonal↗
PubMed1985

A gonadotropin and alpha-subunit suppression test for the assessment of the ectopic production of human chorionic gonadotropin and its subunits after the menopause.

One contraceptive tablet [(CP) containing 0.05 mg ethinyl estradiol and 0.5 mg norgestrel] was administered daily for 7 days to 38 hypergonadotropic postmenopausal women who had benign illness and to 34 similar women with cancer, in order to suppress the gonadotropins (LH and FSH) and their alpha-subunit secreted by the pituitary. LH, FSH, alpha-subunit, and hCG were measured using RIA in serum and urine extracts obtained before and on the seventh day of treatment. In the control group serum alpha-subunit fell to 53%, serum LH to 51%, serum FSH to 36%, urine alpha to 42%, urine hCG to 54%, urine LH to 53%, and urine FSH to 44% of their mean pretreatment values. Serum hCG was undetectable after treatment in all except 11 women in whom serum LH was not adequately suppressed. This fact and the significant positive linear correlation found between basal serum hCG and LH imply that serum hCG measured in postmenopausal women, with a RIA using the SB6 antiserum, is mainly cross-reacting LH. The suppression proved to be useful in the assessment of ectopic production of hCG and its alpha-subunit in the cancer group. Before treatment, 3 patients (8.8%) had elevated serum alpha-subunit levels, whereas after treatment 9 patients (26.5%) had elevated levels. For urine alpha-subunit 3 patients (8.8%) had elevated levels before and 13 (38.2%) after treatment. Six patients (17.7%) had elevated serum hCG levels before and 7 (20.6%) after treatment; however, for urine hCG, 3 patients (9%) had elevated levels before and 8 (24.2%) after treatment. Sephadex G-100 chromatography of urine extracts from two control women showed that the predominant form of free alpha-subunit secreted by the pituitary and excreted in the urine had lower apparent molecular weight after treatment with the CP. Chromatography of urine extracts from two cancer patients demonstrated that a small amount of beta-subunit of hCG produced ectopically by the tumor and excreted into the urine along with a core-type fragment of the hCG-beta was masked in the basal urine by cross-reacting LH; these ectopic peptides were not suppressible and could be specifically measured only after elimination of the urine LH by treatment with the CP. We conclude that administration of contraceptive steroid to post-menopausal women with cancer, by suppressing pituitary gonadotropin secretion and thus minimizing their interference in the hCG RIAs, can be useful in the detection of ectopic production of the hCG and its subunits.

Aged↗
PubMed1992

The expression of human chorionic gonadotropin/human luteinizing hormone receptors in ectopic human endometrial implants.

Our laboratory previously demonstrated that normal human endometrium contains hCG/human LH receptors. Since ectopic endometrial implants in endometriosis arise directly at least in part from uterine endometrium, we investigated whether the implants continue the expression of these receptors. The presence of hCG/LH receptor mRNA and/or immunoreactive receptor protein in ectopic endometrial implants on pelvic peritoneum, uterine endometrium, and unaffected or normal peritoneum from patients with (n = 12) and without (n = 14) clinically apparent endometriosis was examined by in situ hybridization and immunocytochemistry analyses. The results showed that the peritoneal biopsies with visible or microscopic endometrial implants contain receptor mRNA and receptor protein. The glands contain more receptor mRNA and receptor protein than stromal cells in implants similar to uterine endometrium from patients with or without endometriosis. However, there is no consistent difference in the expression of receptors in implants compared to uterine endometria from patients with or without endometriosis. Contrary to ectopic endometrial implants, unaffected or normal peritoneum contain neither receptor mRNA nor receptor protein. In summary, we conclude that ectopic endometrial implants contain hCG/LH receptor mRNA and receptor protein, which suggests new possibilities in the medical treatment of endometriosis.

Adult↗
PubMed2005

Intramedullary ectopic choroid plexus: report of a rare case.

OBJECTIVE AND IMPORTANCE: Intracranial cysts containing an ectopic choroid plexus or choroid plexus-like tissue have seldom been described in the literature. However, there has been no report of a spinal intramedullary cyst containing an ectopic choroid plexus. This is the first case report in the available literature of an ectopic choroid plexus tissue in the spinal cord. CLINICAL PRESENTATION: A 30-year-old man presented with complaints of progressive descending weakness of both upper limbs and increasing stiffness of the lower limbs along with numbness of all four limbs without a history of any bowel or bladder disturbances. Examination was suggestive of a C5-T2 intramedullary lesion. Magnetic resonance imaging revealed a C6-T2 intramedullary cystic lesion along with a small anterosuperiorly placed lesion enhancing with contrast. INTERVENTION: A C6-T2 laminotomy and exploration of the intramedullary cyst and gross total microsurgical excision of the reddish vascular frond-like structure resembling the choroid plexus were performed along with a syringostomy. A laminoplasty with miniplates and screws was performed. Histopathological and immunohistochemical studies revealed a normal choroid plexus. The patient has been followed for 1 year and has demonstrated symptomatic improvement. CONCLUSION: Although there have been rare case reports of drop metastasis of choroid plexus papillomas in the spine, this is the first case report in the available literature of normal but ectopic choroid plexus tissue in the spinal cord.

Adult↗
PubMed2003

Bar homeodomain proteins are anti-proneural in the Drosophila eye: transcriptional repression of atonal by Bar prevents ectopic retinal neurogenesis.

Atonal (Ato)/Math (Mammalian atonal homolog) family proneural proteins are key regulators of neurogenesis in both vertebrates and invertebrates. In the Drosophila eye, Ato is essential for the generation of photoreceptor neurons. Ato expression is initiated at the anterior ridge of the morphogenetic furrow but is repressed in the retinal precursor cells behind the furrow to prevent ectopic neurogenesis. We show that Ato repression is mediated by the conserved homeobox proteins BarH1 and BarH2. Loss of Bar causes cell-autonomous ectopic Ato expression, resulting in excess photoreceptor clusters. The initial ommatidial spacing at the furrow occurs normally in the absence of Bar, suggesting that the ectopic neurogenesis within Bar mutant clones is not due to the lack of Notch (N)-dependent lateral inhibition. Targeted misexpression of Bar is sufficient to repress ato expression. Furthermore, we provide evidence that Bar represses ato expression at the level of transcription without affecting the expression of an ato activator, Cubitus interruptus (Ci). Thus, we propose that Bar is essential for transcriptional repression of ato and the prevention of ectopic neurogenesis behind the furrow.

Animals↗
PubMed2003

The pro-apoptotic gene Bax is required for the death of ectopic primordial germ cells during their migration in the mouse embryo.

In the mouse embryo, significant numbers of primordial germ cells (PGCs) fail to migrate correctly to the genital ridges early in organogenesis. These usually die in ectopic locations. In humans, 50% of pediatric germ line tumors arise outside the gonads, and these are thought to arise from PGCs that fail to die in ectopic locations. We show that the pro-apoptotic gene Bax, previously shown to be required for germ cell death during later stages of their differentiation in the gonads, is also expressed during germ cell migration, and is required for the normal death of germ cells left in ectopic locations during and after germ cell migration. In addition, we show that Bax is downstream of the known cell survival signaling interaction mediated by the Steel factor/Kit ligand/receptor interaction. Together, these observations identify the major mechanism that removes ectopic germ cells from the embryo at early stages.

Animals↗
PubMed1992

Exogenous retinoic acid rapidly induces anterior ectopic expression of murine Hox-2 genes in vivo.

Exogenous retinoic acid (RA) has teratogenic effects on vertebrate embryos and alters Hox-C gene expression in vivo and in vitro. We wish to examine whether RA has a role in the normal regulation of Hox-C genes, and whether altered Hox-C gene expression in response to RA leads to abnormal morphology. The expression of 3' Hox-2 genes (Hox-2.9, Hox-2.8, Hox-2.6 and Hox-2.1) and a 5' gene (Hox-2.5) were examined by whole-mount in situ hybridization on embryos 4 hours after maternal administration of teratogenic doses of RA on embryonic day 7 to 9. The expression of the 3' Hox-2 genes was found to be ectopically induced in anterior regions in a stage-specific manner. The Hox-2.9 and Hox-2.8 genes were induced anteriorly in the neurectoderm in response to RA on day 7 but not at later stages. Expression of Hox-2.6 and Hox-2.1 was ectopically induced anteriorly in neurectoderm in response to RA on day 8. Hox-2.1 remained responsive on day 9, whereas Hox-2.6 was no longer responsive at this stage. The expression of the 5' gene Hox-2.5 was not detectably altered at any of these stages by RA treatments. We also examined the response of other genes whose expression is spatially regulated in early embryos. The expression of En-2 and Wnt-7b was not detectably altered by RA, whereas RAR beta expression was induced anteriorly by RA on day 7 and 8. Krox-20 expression was reduced in a stage- and region-specific manner by RA. The ectopic anterior expression of Hox-2.8 and Hox-2.9 induced by RA on day 7 was persistent to day 8, as was the altered expression of Krox-20. The altered pattern of expression of these genes in response to RA treatment on day 7 may be indicative of a transformation of anterior hindbrain to posterior hindbrain, specifically, a transformation of rhombomeres 1 to 3 towards rhombomere 4 identity with an anterior expansion of rhombomere 5. The ectopic expression of the 3' Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3' Hox-C gene expression boundaries early in development.

Animals↗
PubMed1998

Correlation of wing-leg identity in ectopic FGF-induced chimeric limbs with the differential expression of chick Tbx5 and Tbx4.

It has been reported that members of the fibroblast growth factor (FGF) family can induce additional limb formation in the flank of chick embryos. The phenotype of the ectopic limb depends on the somite level at which it forms: limbs in the anterior flank resemble wings, whereas those in the posterior flank resemble legs. Ectopic limbs located in the mid-flank appear chimeric, possessing characteristics of both wings and legs; feather buds are present in the anterior halves with scales and claws in the posterior halves. To study the mechanisms underlying the chimerism of these additional limbs, we cloned chick Tbx5 and Tbx4 to use as forelimb and hindlimb markers and examined their expression patterns in FGF-induced limb buds. We found that Tbx5 and Tbx4 were differentially expressed in the anterior and posterior halves of additional limb buds in the mid-flank, respectively, consistent with the chimeric patterns of the integument. A boundary of Tbx5/Tbx4 exists in all ectopic limbs, indicating that the additional limbs are essentially chimeric, although the degree of chimerism is dependent on the position. The boundary of Tbx5/Tbx4 expression is not fixed at a specific position within the interlimb region, but dependent upon where FGF was applied. Since the ectopic expression patterns of Tbx5/Tbx4 in the additional limbs are closely correlated with the patterns of their chimeric phenotypes, it is likely that Tbx5 and Tbx4 expression in the limb bud is involved in determination of the forelimb and hindlimb identities, respectively, in vertebrates.

Amino Acid Sequence↗
PubMed1999

The midbrain-hindbrain boundary genetic cascade is activated ectopically in the diencephalon in response to the widespread expression of one of its components, the medaka gene Ol-eng2.

In vertebrates, the engrailed genes are expressed at early neurula stage in a narrow stripe encompassing the midbrain-hindbrain boundary (MHB), a region from which a peculiar structure, the isthmus, is formed. Knock-out experiments in mice demonstrated that these genes are essential for the development of this structure and of its derivatives. In contrast, little is known about the effect of an overexpression of engrailed genes in vertebrate development. Here we report the isolation of Ol-eng2, a medaka fish (Oryzias latipes) engrailed gene. We have monitored the effects of its widespread expression following mRNA injections in 1- and 2-cell medaka and Xenopus embryos. We found that the ectopic expression of Ol-eng2 predominantly results in an altered development of the anterior brain, including an inhibition of optic vesicle formation. No change in the patterns of mesencephalic and telencephalic markers were observed. In contrast, expressions of markers of the diencephalon were strongly repressed in injected embryos. Furthermore, the endogenous Ol-eng2, Pax2, Wnt1 and Fgf8, which are essential components of the MHB genetic cascade, were ectopically expressed in this region. Therefore, we propose that Ol-eng2 induces de novo formation of an isthmus-like structure, which correlates with the development of ectopic midbrain structures, including optic tectum. A competence of the diencephalon to change to a midbrain fate has been demonstrated in isthmic graft experiments. Our data demonstrate that this change can be mimicked by ectopic engrailed expression alone.

Amino Acid Sequence↗
PubMed2000

The Drosophila homeobox gene optix is capable of inducing ectopic eyes by an eyeless-independent mechanism.

optix is a new member of the Six/so gene family from Drosophila that contains both a six domain and a homeodomain. Because of its high amino acid sequence similarity with the mouse Six3 gene, optix is considered to be the orthologous gene from Drosophila rather than sine oculis, as previously believed. optix expression was detected in the eye, wing and haltere imaginal discs. Ectopic expression of optix leads to the formation of ectopic eyes suggesting that optix has important functions in eye development. Although optix and sine oculis belong to the same gene family (Six/so) and share a high degree of amino acid sequence identity, there are a number of factors which suggest that their developmental roles are different: (1) the expression patterns of optix and sine oculis are clearly distinct; (2) sine oculis acts downstream of eyeless, whereas optix is expressed independently of eyeless; (3) sine oculis functions synergistically with eyes absent in eye development whereas optix does not; (4) ectopic expression of optix alone, but not of sine oculis can induce ectopic eyes in the antennal disc. These results suggest that optix is involved in eye morphogenesis by an eyeless-independent mechanism.

Amino Acid Sequence↗