Activating and repressing signals in head development: the role of Xotx1 and Xotx2

Development ◽  
1997 ◽  
Vol 124 (9) ◽  
pp. 1733-1743 ◽  
Author(s):  
M. Andreazzoli ◽  
M. Pannese ◽  
E. Boncinelli
Keyword(s):  
Retinoic Acid ◽  
Ectopic Expression ◽  
Convergent Extension ◽  
Negative Interference ◽  
Head Development ◽  
Tail Development ◽  
Head Formation ◽  
Organizer Activity ◽  
Tail Organizer

Xotx1 and Xotx2 are two Xenopus homologues of the Drosophila orthodenticle gene that are specifically expressed in presumptive head regions that do not undergo convergent extension movements during gastrulation. We studied the function of Xotx1 and compared it with that of Xotx2. Ectopic expression of each of the two genes has similar effects in impairing trunk and tail development. Experimental evidence suggests that posterior deficiencies observed in microinjected embryos are due to negative interference with convergent extension movements. Transplantations of putative tail-forming regions showed that, while Xotx1 overexpression inhibits tail organizer activity, Xotx2 overexpression is able to turn a tail organizer into a head organizer. Finally, Xotx1 and Xotx2 are activated by factors involved in head formation and repressed by a posteriorizing signal like retinoic acid. Taken together, these data suggest that Xotx genes are involved in head-organizing activity. They also suggest that the head organizer may act not only stimulating the formation of anterior regions, but also repressing the formation of posterior structures.

A role for the vegetally expressed Xenopus gene Mix.1 in endoderm formation and in the restriction of mesoderm to the marginal zone

Development ◽  
1998 ◽  
Vol 125 (13) ◽  
pp. 2371-2380 ◽  
Author(s):  
P. Lemaire ◽  
S. Darras ◽  
D. Caillol ◽  
L. Kodjabachian
Keyword(s):  
Marginal Zone ◽  
Ectopic Expression ◽  
Homeobox Gene ◽  
Early Response ◽  
Endoderm Differentiation ◽  
Head Formation ◽  
Mutual Repression ◽  
Regulatory Loop ◽  
Strong Activator

We have studied the role of the activin immediate-early response gene Mix.1 in mesoderm and endoderm formation. In early gastrulae, Mix.1 is expressed throughout the vegetal hemisphere, including marginal-zone cells expressing the trunk mesodermal marker Xbra. During gastrulation, the expression domains of Xbra and Mix.1 become progressively exclusive as a result of the establishment of a negative regulatory loop between these two genes. This mutual repression is important for the specification of the embryonic body plan as ectopic expression of Mix.1 in the Xbra domain suppresses mesoderm differentiation. The same effect was obtained by overexpressing VP16Mix.1, a fusion protein comprising the strong activator domain of viral VP16 and the homeodomain of Mix.1, suggesting that Mix.1 acts as a transcriptional activator. Mix.1 also has a role in endoderm formation. It cooperates with the dorsal vegetal homeobox gene Siamois to activate the endodermal markers edd, Xlhbox8 and cerberus in animal caps. Conversely, vegetal overexpression of enRMix.1, an antimorphic Mix.1 mutant, leads to a loss of endoderm differentiation. Finally, by targeting enRMix.1 expression to the anterior endoderm, we could test the role of this tissue during embryogenesis and show that it is required for head formation.

Developmental role of endogenous retinoids in the determination of morphallactic field in budding tunicates

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 835-845 ◽  
Author(s):  
K. Kawamura ◽  
K. Hara ◽  
S. Fujiwara
Keyword(s):  
Retinoic Acid ◽  
Aldehyde Dehydrogenase ◽  
Ectopic Expression ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Proximal Extremity ◽  
Developmental Role

We have extracted retinoids from the budding tunicate Polyandrocarpa misakiensis and, using HPLC, identified some major peaks as cis-retinal, all-trans-retinal and all-trans-retinoic acid, of which cis-retinal was most abundant (~2 micromolar). In developing buds, the amount of cis-retinal was about one-fifth that of the adult animals. In those buds, aldehyde dehydrogenase, which could metabolize retinal in vitro, was expressed in epithelial cells and then in mesenchymal cells at the proximal extremity, that is, the future developmental field of the bud. Exogenous retinoic acid comparable to the endogenous level could induce an additional field at the distal end of the bud, resulting in a double monster. The induction always accompanied an ectopic expression of aldehyde dehydrogenase. The results of this work suggest that retinoic acid or related molecule(s) act as an endogenous trigger of morphallactic development of Polyandrocarpa buds.

Evidence of a role for endogenous electrical fields in chick embryo development

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 985-996 ◽  
Author(s):  
K.B. Hotary ◽  
K.R. Robinson
Keyword(s):  
Chick Embryo ◽  
Internal Field ◽  
Limb Bud ◽  
Control Group ◽  
Electrical Fields ◽  
Head Development ◽  
Tail Development ◽  
Experimental Group ◽  
Common Defect

We have tested directly the hypothesis that the endogenous electrical field in the chick embryo plays a causal role in development. Conductive implants, which shunt currents out of the embryo and thus alter the internal field, were placed under the dorsal skin at the mid-trunk level of stage 11–15 embryos. Currents leaving the posterior intestinal portal (p.i.p.) of these embryos were reduced by an average of 30%. Control embryos receiving non-conductive implants showed no change in p.i.p. currents. In the group receiving current shunts, 92% of the embryos exhibited some developmental abnormality. Only 11% of the control group displayed defects. The most common defect in the experimental group (81%) was in tail development. Tail defects ranged from complete absence to the formation of a normal length, but morphologically abnormal tail. Internally, tail structures (neural tube, notochord and somites) were frequently absent or aberrantly formed. In 33% of the experimental embryos, the notochord continued lengthening in the absence of any other tail development. This led to the formation of ourenteric outgrowths from the hindgut. Defects in limb bud and head development were also found in experimentally treated embryos, but at a much lower frequency than tail defects. The abnormalities observed in experimental embryos were very similar to those produced naturally in rumpless mutant chicks. A vibrating probe analysis of these mutants (from both dominant and recessive strains) showed that currents leaving the p.i.p. were significantly lower in phenotypically abnormal mutants than in wild-type and phenotypically normal mutant embryos from both strains. There was no apparent correlation between the average transepithelial potential (TEP) of these mutants and the development of tail abnormalities. The possible role of endogenous electrical fields in chick tail development is discussed.

Defective lens fiber differentiation and pancreatic tumorigenesis caused by ectopic expression of the cellular retinoic acid-binding protein I

Development ◽  
1993 ◽  
Vol 119 (2) ◽  
pp. 363-375
Author(s):  
A.V. Perez-Castro ◽  
V.T. Tran ◽  
M.C. Nguyen-Huu
Keyword(s):  
Retinoic Acid ◽  
Binding Proteins ◽  
Binding Protein ◽  
Ectopic Expression ◽  
Retinoic Acid Receptors ◽  
Acid Binding Protein ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Retinoic Acid Binding Proteins

All-trans retinoic acid, a metabolite of retinol, is a possible morphogen in vertebrate development. Two classes of cellular proteins, which specifically bind all-trans retinoic acid, are thought to mediate its action: the nuclear retinoic acid receptors (RAR alpha, beta, gamma), and the cytoplasmic binding proteins known as cellular retinoic acid-binding proteins I and II (CRABP I and II). The function of the retinoic acid receptors is to regulate gene transcription by binding to DNA in conjunction with the nuclear retinoid X receptors (RXR alpha, beta, gamma), which in turn have 9-cis retinoic acid as a ligand. Several lines of evidence suggest that the role of the cellular retinoic acid-binding proteins is to control the concentration of free retinoic acid reaching the nucleus in a given cell. Here, we have addressed the role of the cellular retinoic acid-binding protein I in development by ectopically expressing it in the mouse lens, under the control of the alpha A-crystallin promoter. We show that this ectopic expression interferes with the development of the lens and with the differentiation of the secondary lens fiber cells, causing cataract formation. These results suggest that correct regulation of intracellular retinoic acid concentration is required for normal eye development. In addition, the generated transgenic mice also present expression of the transgene in the pancreas and develop pancreatic carcinomas, suggesting that overexpression of the cellular retinoic acid-binding protein is the cause of the tumors. These results taken together provide evidence for a role of the cellular retinoic acid-binding protein in development and cell differentiation. The relevance of these findings to the possible role of the cellular retinoic acid-binding proteins in the transduction of the retinoic acid signal is discussed.

scholarly journals Active repression by unliganded retinoid receptors in development

2003 ◽  
Vol 161 (2) ◽  
pp. 223-228 ◽  
Author(s):  
Andrea D. Weston ◽  
Bruce Blumberg ◽  
T. Michael Underhill
Keyword(s):  
Retinoic Acid ◽  
Cell Fate ◽  
Thyroid Hormone Receptor ◽  
Trichostatin A ◽  
Skeletal Development ◽  
Dominant Negative ◽  
Retinoid Receptors ◽  
Head Formation ◽  
Developmental Role

The retinoid receptors have major roles throughout development, even in the absence of ligand. Here, we summarize an emerging theme whereby gene repression, mediated by unliganded retinoid receptors, can dictate cell fate. In addition to activating transcription, retinoid receptors actively repress gene transcription by recruiting cofactors that promote chromatin compaction. Two developmental processes for which gene silencing by the retinoid receptors is essential are head formation in Xenopus and skeletal development in the mouse. Inappropriate repression, by oncogenic retinoic acid (RA)**Abbreviations used in this paper: APL, acute promyelocytic leukemia; dnRARα, dominant–negative version of the RARα; E, embryonic age; HDAC, histone deacetylase; LCoR, ligand-dependent corepressor; NCoR, nuclear receptor corepressor; RA, retinoic acid; RAR, RA receptor; RARE, RXR homodimer bound to bipartite response element; RXR, retinoid X receptor; TSA, trichostatin A; CYP26, cytochrome p450, 26; TR, thyroid hormone receptor. receptor (RAR) fusion proteins, blocks myeloid differentiation leading to a rare form of leukemia. Our current understanding of the developmental role of retinoid repression and future perspectives in this field are discussed.

Retinoic acid modifies development of the midbrain-hindbrain border and affects cranial ganglion formation in zebrafish embryos

Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1159-1170 ◽  
Author(s):  
N. Holder ◽  
J. Hill
Keyword(s):  
Retinoic Acid ◽  
Neural Development ◽  
Neuronal Development ◽  
Expression Domain ◽  
Head Development ◽  
Cranial Ganglia ◽  
Cranial Ganglion ◽  
Neural Anatomy ◽  
Distinct Features

Considerable evidence now suggests that retinoic acid (RA) is an important modulator of patterning events in early neuronal development in vertebrates. In this paper, we describe the effects of exogenously applied RA on early neural development in the zebrafish embryo. Neural anatomy is assessed by immunocytochemical and histochemical analysis of the developing embryo in whole mounts at 24 h post-fertilization. RA was applied for one hour at concentrations ranging from 10(−9) to 10(−6) M to embryos at 50% epiboly, the midgastrula stage, and at 10(−7) M to embryos at early and late gastrula stages. The neuroanatomical analysis shows that 10(−7) M RA causes a defined lesion to the developing central nervous system which corresponds to a loss of a region of the brain in the caudal midbrain-rostral hindbrain area, the precursor of the cerebellum and associated neural structures. The region that fails to develop corresponds to the cranial expression domain of the engrailed protein as assessed by the monoclonal antibody 4D9 (Patel et al. 1989: Expression of engrailed proteins in arthropods, annelids and chordates. Cell 58, 955–968). Structures caudal to rhombomere 4 are unaffected by 10(−7) M RA, as are the cranial midbrain and forebrain: 10(−7) M RA also affects the development of cranial ganglia, principally the Vth, anterior lateral line and VIIIth ganglia, suggesting that RA affects normal development of the cranial neural crest. Effects of RA at stages immediately prior to and after gastrulation show some similar and some distinct features. Results are discussed in terms of the possible role of RA as an endogenous moderator of normal head development.

scholarly journals Regulatory role of G9a and LSD1 in the Transcription of Olfactory Receptors during Leukaemia Cell Differentiation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hyeonsoo Jung ◽  
Yun-Cheol Chae ◽  
Ji-Young Kim ◽  
Oh-Seok Jeong ◽  
Hoon Kook ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Ectopic Expression ◽  
Olfactory Receptors ◽  
Leukaemia Cell ◽  
Leukaemia Cell Line ◽  
Different Types ◽  
Olfactory Cells ◽  
And Function

Abstract Recent studies have reported the ectopic expression of olfactory receptors (ORs) in non-olfactory tissues, however, their physiological roles were not well elucidated. ORs are expressed in and function in different types of cancers. Here, we identified that the H3K9me2 levels of several OR promoters decreased during differentiation in the HL-60, human myeloid leukaemia cell line, by all-trans-retinoic acid (ATRA). We found that the differential OR promoters H3K9me2 levels were regulated by G9a and LSD1, resulting in the decrease of ORs transcription during HL-60 differentiation. G9a and LSD1 could regulate the expression of ORs in several non-olfactory cells via the methylation and demethylation of H3K9me2. In addition, we demonstrated that knockdown of OR significantly reduced cell proliferation. Therefore, the epigenetic regulation of ORs transcription is critical for carcinogenesis.

Ectopic expression of Hoxa-1 in the zebrafish alters the fate of the mandibular arch neural crest and phenocopies a retinoic acid-induced phenotype

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 735-746 ◽  
Author(s):  
D. Alexandre ◽  
J.D. Clarke ◽  
E. Oxtoby ◽  
Y.L. Yan ◽  
T. Jowett ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Ectopic Expression ◽  
Head Region ◽  
Hox Gene ◽  
Abnormal Growth ◽  
Primary Body ◽  
Arch Neural ◽  
The Relationship

Considerable evidence has demonstrated that retinoic acid influences the formation of the primary body axis in vertebrates and that this may occur through the regulation of Hox gene expression. In this study, we show that the phenotype induced by exogenous retinoic acid in the zebrafish can also be generated by the overexpression of Hoxa-1 following injection of synthetic RNA into the fertilised egg. The isolation, sequence and expression pattern of the zebrafish Hoxa-1 gene is described. We show that exogenously applied retinoic acid causes the ectopic accumulation of Hoxa-1 message during gastrulation in the hypoblast in the head region. Overexpression of Hoxa-1 following injection of RNA causes abnormal growth of the anterior hindbrain, duplication of Mauthner neurons in rhombomere (r) 2 and fate changes of r2 mesenchymal and neurogenic neural crest. These results are discussed in terms of the role of Hoxa-1 in controlling anterior hindbrain patterning and the relationship between expression of Hoxa-1 and retinoic acid.

scholarly journals Florigen governs shoot regeneration

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yaarit Kutsher ◽  
Michal Fisler ◽  
Adi Faigenboim ◽  
Moshe Reuveni
Keyword(s):  
Nitric Oxide ◽  
Shoot Regeneration ◽  
Ectopic Expression ◽  
Flowering Plants ◽  
Regeneration Capacity ◽  
No Donor ◽  
Tobacco Leaves ◽  
Age Related ◽  
Delayed Flowering

AbstractIt is widely known that during the reproductive stage (flowering), plants do not root well. Most protocols of shoot regeneration in plants utilize juvenile tissue. Adding these two realities together encouraged us to study the role of florigen in shoot regeneration. Mature tobacco tissue that expresses the endogenous tobacco florigen mRNA regenerates poorly, while juvenile tissue that does not express the florigen regenerates shoots well. Inhibition of Nitric Oxide (NO) synthesis reduced shoot regeneration as well as promoted flowering and increased tobacco florigen level. In contrast, the addition of NO (by way of NO donor) to the tissue increased regeneration, delayed flowering, reduced tobacco florigen mRNA. Ectopic expression of florigen genes in tobacco or tomato decreased regeneration capacity significantly. Overexpression pear PcFT2 gene increased regeneration capacity. During regeneration, florigen mRNA was not changed. We conclude that florigen presence in mature tobacco leaves reduces roots and shoots regeneration and is the possible reason for the age-related decrease in regeneration capacity.

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