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Homeotic Transformation (homeotic + transformation)
Selected AbstractsRetinoic acid affects craniofacial patterning by changing Fgf8 expression in the pharyngeal ectodermDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 9 2008Makoto Abe Retinoic acid signaling plays important roles in establishing normal patterning and cellular differentiation during embryonic development. In this study, we show that single administration of retinoic acid at embryonic day 8.5 causes homeotic transformation of the lower jaw into upper jaw-like structures. This homeosis was preceded by downregulation of Fgf8 and Sprouty expression in the proximal domain of the first pharyngeal arch. Downregulation of mesenchymal genes such as Dlx5, Hand2, Tbx1 and Pitx2 was also observed. The oropharynx in retinoic acid-treated embryos was severely constricted. Consistent with this observation, Patched expression in the arch endoderm and mesenchyme was downregulated. Thus, retinoic acid affects the expression of subsets of epithelial and mesenchymal genes, possibly disrupting the regional identity of the pharyngeal arch. [source] All- trans retinoic acid-induced ectopic limb and caudal structures: Murine strain sensitivities and pathogenesisDEVELOPMENTAL DYNAMICS, Issue 6 2008Xiaoyan Liao Abstract Treatment of pregnant mice at the egg cylinder stage with retinoic acid (RA) has caused ectopic hindlimbs in the offspring. Proposed causes of ectopic hindlimbs include homeotic transformation or multiple axis formation. Two mouse strains were determined to be divergent in susceptibility to this malformation (C57BL/6N, highly sensitive; SWV/Fnn, less sensitive). Ectopic limbs were hindlimbs (expressing Pitx1 and Tbx4 but not Tbx5), yet they also expressed the predominantly forelimb Hoxb8. Ectopic body axis formation was indicated by gene expression for ectopic primitive streaks, notochords, and nodes, as well as inhibition of anterior visceral endoderm and mesodermal migration. The earlier in development that embryos were examined, the higher the rate of ectopic hindlimb development and axis formation. Ectopic axis formation and cell migration inhibition had the same strain susceptibility as the dysmorphogenesis. We propose that all extra hindlimbs were derived from ectopic axis formation, perturbation of which is genetic background dependent. Developmental Dynamics 237:1553,1564, 2008. © 2008 Wiley-Liss, Inc. [source] High assimilation of the sacrum in a sample of American skeletons: Prevalence, pelvic size, and obstetrical and evolutionary implicationsAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 4 2009Robert G. Tague Abstract High assimilation sacrum is fusion of the caudal-most lumbar vertebra to the first sacral vertebra. Previous studies have shown that high assimilation is associated with clinical problems, including obstetrical difficulty. This study used adult American males (n = 1,048) and females (n = 1,038) of the Hamann,Todd and Terry skeletal collections to determine the prevalence of high assimilation and its effect on pelvic size, and to consider the obstetrical and evolutionary implications of high assimilation. The prevalence of high assimilation in this sample is 6.3%, with males and females not differing significantly from one another in their prevalence. This prevalence is near the median for that reported in 41 other samples. In both males and females, individuals with high assimilation have significantly longer anteroposterior and posterior sagittal diameters of the inlet, and shorter sacrum compared to those with a nonassimilated sacrum. Females with high assimilation have a significantly narrower sacral angulation (i.e., reduced inclination of ventral axis of sacrum), and shorter posterior sagittal diameter of the outlet compared to those with a nonassimilated sacrum. A short posterior sagittal diameter of the outlet is associated with childbirth difficulty. As high assimilation is partial homeotic transformation of a lumbar vertebra, this study supports previous research that homeotic transformation of vertebrae is selectively disadvantageous. Am J Phys Anthropol, 2009. © 2008 Wiley-Liss, Inc. [source] "Mir"acles in hox gene regulationBIOESSAYS, Issue 5 2006Vivek S. Chopra Micro RNAs (miRNAs) have been shown to control many cellular processes including developmental timing in different organisms. The prediction that miRNAs are involved in regulating hox genes of flies and mouse is quite a recent idea and is supported by the finding that mir-196 represses Hoxb8 gene expression. The non-coding regions that encode these miRNAs are also conserved across species in the same way as other mechanisms that regulate expression of hox genes. On the contrary, until now no homeotic phenotype, a hallmark of any hox gene mutation, had been associated with any hox miRNA. Recent work on bithorax complex miRNA (miR,iab-4,5p) shows, for the first time, that miRNAs can lead to homeotic transformation. This miRNA regulates Ultrabithorax (Ubx) and results in the transformation of haltere to wing.1 This study unveils a new complexity and finesse to the regulation of hox gene expression pattern that is needed for determining the anteroposterior body axis in all bilaterians. BioEssays 28: 445,448, 2006. © 2006 Wiley Periodicals, Inc. [source] Stem cells and gastric cancer: Role of gastric and intestinal mixed intestinal metaplasiaCANCER SCIENCE, Issue 2 2003Masae Tatematsu All of the different types of stomach epithelial cells are known to be derived from a single progenitor cell in each gland. Similarly, cancers develop from single cells, based on data from clonality analysis in C3H/HeN , BALB/c chimeric mice. Using gastric and intestinal epithelial cell markers, intestinal metaplasia (IM) can be divided into two major types: a gastric and intestinal (GI) mixed type, and a solely intestinal (I) type. Ectopic expression of Cdx genes and down-regulation of Sox2 in isolated single GI mixed IM glands suggests abnormal differentiation of stem cells that can produce both gastric (G) and I type cells. Similarly, phenotypic expression of gastric cancer cells of each histological type can be clearly classified into G and I type epithelial cells. The heterogeneity of phenotypic expression of gastric cancer cells in individual cancers is assumed to reflect this intrinsic potential for differentiation in two directions. Gastric cancers at early stages, independent of the histological type, mainly consist of G type cells, and phenotypic shift from G to I type expression is clearly observed with progression. The data thus suggest IM may not be a preneoplastic change in gastric carcinoma, but rather that cells of the I type may appear independently in the gastric mucosa in IM and in gastric cancers. Intestinalization of gastric mucosa and cancer cells may represent a kind of homeotic transformation. Whether disturbance of the regulation of Sox2 and Cdx genes may be of importance to the biological behavior of gastric cancers should therefore be clarified in future studies. (Cancer Sci 2003; 94: 135,141) [source] Drosophila female sterile (1) homeotic is a multifunctional transcriptional regulator that is modulated by Ras signalingDEVELOPMENTAL DYNAMICS, Issue 3 2008Brian L. Florence Abstract The Drosophila (fs(1)h) gene encodes small (Fs(1)hS) and large (Fs(1)hL) chromatin-binding BET protein transcription factor isoforms. Zygotic mutations cause either lethality or female sterility, whereas maternal mutations cause segmental deletions and thoracic homeotic transformations. Here, we describe novel fs(1)h embryonic phenotypes: homeosis of the head in zygotic mutants and deletion of head and tail regions in maternal mutants, similar to those caused by dominant torso (torD) alleles. tor activates transcription of tailless (tll) and hückebein (hkb) by means of a canonical Ras pathway, through inactivation of Groucho (Gro), Capicua (Cic) and, possibly, Grainy-head (Grh) repressors. Expression of both tailless and hückebein are de-repressed in fs(1)h maternal mutants, as in torD, gro, grh, and cic mutant animals, indicating fs(1)h is also necessary for tll and hkb repression. These data link Ras signaling with modulation of a chromatin-binding transcription factor, Fs(1)h, suggesting a novel mechanism by which Ras can modulate gene expression. Developmental Dynamics 237:554,564, 2008. © 2008 Wiley-Liss, Inc. [source] Defects in cervical vertebrae in boric acid-exposed rat embryos are associated with anterior shifts of hox gene expression domainsBIRTH DEFECTS RESEARCH, Issue 1 2003Nathalie Wéry BACKGROUND Previously, we showed that prenatal exposure to boric acid (BA), an industrial agent with large production, causes alterations of the axial skeleton in rat embryos, reminiscent of homeotic transformations. Indeed, Sprague-Dawley rats exposed in utero to BA on gestation day 9 (GD 9) had only six, rather than the normal seven, cervical vertebrae. This finding, observed in 91% of GD 21 fetuses, suggests posterior transformations of vertebrae. The present study attempts to determine if these skeletal alterations could be explained by modifications of the hox code, involved in the establishment of positional information along the craniocaudal axis of the embryo. METHODS Pregnant rats were treated by gavage with BA (500 mg/kg, twice) on GD 9. Embryos were collected on GD 11 or GD 13.5 and processed for in situ hybridization. Several hox genes were selected according to the position of their cranial limit of expression in the cervical and thoracic region. RESULTS At GD 13.5, we detected a cranial shift of the anterior limit of expression of hoxc6 and hoxa6. We observed no difference between control and treated embryos in the location of the cranial limit of expression of the other genes: hoxd4, hoxa4, hoxc5, and hoxa5. CONCLUSIONS Our results demonstrate that following in utero exposure to BA on GD 9, a disturbance of the expression of hox genes involved in the specification of most anterior vertebrae is observed at GD 13.5. Based on their expression domain and on their implication in the definition of the cervicothoracic vertebral boundary, it is likely that the anteriorization of hoxc6 and hoxa6 reported here is correlated to the morphological phenotype observed in BA-exposed fetuses at GD 21. Birth Defects Research (Part A) 67:59,67, 2003. © 2003 Wiley-Liss, Inc. [source] THIS ARTICLE HAS BEEN RETRACTED Epigenetic regulator polycomb group protein complexes control cell fate and cancerCANCER SCIENCE, Issue 6 2008Rieko Kanno The chromatin-associated Polycomb group (PcG) proteins were first identified in genetic screens for homeotic transformations in Drosophila melanogaster. Besides body patterning, members of the PcG are now known to regulate epigenetic cellular memory, stem cell self-renewal, and cancer development. Here, we discuss the multifarious functions of the PcG family, isoforms of protein complexes, and its enzymatic activities, for example histone methylation, links to DNA methylation, its phosphorylation status, H2A mono-ubiquitination, SUMOylation, and links to non-coding RNA. We also discuss the function of cytosolic PcG complexes as a regulator of receptor-induced actin polymerization and proliferation in a methylation-dependent manner. We propose that the functional versatility of PcG protein complexes contributed significantly to the complexity of heritable gene repression mechanisms, signal transduction, and cell proliferation in cancer development. (Cancer Sci 2008; 99: 1077,1084) [source] | ||||||||||