The ventral and posterior expression of the zebrafish homeobox gene eve1 is perturbed in dorsalized and mutant embryos

Development ◽  
1993 ◽  
Vol 119 (4) ◽  
pp. 1261-1275 ◽  
Author(s):  
J.S. Joly ◽  
C. Joly ◽  
S. Schulte-Merker ◽  
H. Boulekbache ◽  
H. Condamine
Keyword(s):  
Cell Fate ◽  
Zebrafish Embryo ◽  
Marginal Zone ◽  
Posterior Part ◽  
Homeobox Gene ◽  
Migratory Behaviour ◽  
Wild Type ◽  
Tail Region ◽  
Expression Domain ◽  
Tail Tip

We have identified and characterized zebrafish eve1, a novel member of the Drosophila even-skipped (eve) gene family. eve1 RNAs are expressed initially in late blastulae with a peak during the gastrula stage, at which time expression is confined to ventral and lateral cells of the marginal zone of the zebrafish embryo. Later, eve1 transcripts are located in the most posterior part of the extending tail tip. We show that LiCl, known to dorsalize Xenopus embryos, has the same effect in zebrafish, resulting in embryos with exaggerated dorsoanterior structures. In LiCl-treated embryos, eve1 transcripts are completely absent. eve1 is therefore a marker of ventral and posterior cells. In the light of its ventroposterior expression domain, the localization of eve1 transcripts was analysed in spadetail (spt) and no tail (ntl), two mutants with abnormal caudal development. In sptb140 homozygous mutants, there is an accumulation of cells in the tail region, resulting from inadequate migratory behaviour of precursors to the trunk somites. These cells, in their abnormal environment, express eve1, emphasizing the correlation between ventroposterior position and eve1 expression. In homozygous mutant embryos for the gene ntl (the homologue of mouse Brachyury, originally called Zf-T), posterior structures are missing (M. E. Halpern, C. B. Kimmel, R. K. Ho and C. Walker, 1993; Cell In press). While mutant and wild-type embryos do not differ in their eve1 transcript distribution during gastrulation, eve1 expression is absent in the caudal region of mutant ntl embryos during early somitogenesis, indicating a requirement for ntl in the maintenance of eve1 expression during tail extension. Our findings suggest that eve1 expression is correlated with a ventral and posterior cell fate, and provide first insights into its regulation.

scholarly journals Antimorphic goosecoids

Development ◽  
1998 ◽  
Vol 125 (8) ◽  
pp. 1347-1359 ◽  
Author(s):  
B. Ferreiro ◽  
M. Artinger ◽  
K. Cho ◽  
C. Niehrs
Keyword(s):  
Transcriptional Activation ◽  
Low Dose ◽  
Marginal Zone ◽  
Homeobox Gene ◽  
Axis Formation ◽  
Wild Type ◽  
Transcriptional Activation Domain ◽  
Spemann Organizer ◽  
Axial Defects ◽  
Dorsal Mesoderm

goosecoid (gsc) is a homeobox gene expressed in the Spemann organizer that has been implicated in vertebrate axis formation. Here antimorphic gscs are described. One antimorphic gsc (MTgsc) was fortuitously created by adding 5 myc epitopes to the N terminus of gsc. The other antimorph (VP16gsc) contains the transcriptional activation domain of VP16. mRNA injection of either antimorph inhibits dorsal gastrulation movements and leads to embryos with severe axial defects. They upregulate ventral gene expression in the dorsal marginal zone and inhibit dorsal mesoderm differentiation. Like the VP16 domain, the N-terminal myc tags act by converting wild-type gsc from a transcriptional repressor into an activator. However, unlike MTgsc, VP16gsc is able at low dose to uncouple head from trunk formation, indicating that different antimorphs may elicit distinct phenotypes. The experiments reveal that gsc and/or gsc-related genes function in axis formation and gastrulation. Moreover, this work warns against using myc tags indiscriminately for labeling DNA-binding proteins.

Sectors expressing the homeobox gene liguleless3 implicate a time-dependent mechanism for cell fate acquisition along the proximal-distal axis of the maize leaf

Development ◽  
1997 ◽  
Vol 124 (24) ◽  
pp. 5097-5106 ◽  
Author(s):  
G.J. Muehlbauer ◽  
J.E. Fowler ◽  
M. Freeling
Keyword(s):  
Cell Fate ◽  
Homeobox Gene ◽  
Longitudinal Axis ◽  
Cell Types ◽  
Transverse Dimension ◽  
Leaf Sheath ◽  
Wild Type ◽  
Cell Fates ◽  
Maize Leaf ◽  
Gradual Process

The longitudinal axis of the maize leaf is composed of, in proximal to distal order, sheath, ligule, auricle and blade. The semidominant Liguleless3-O (Lg3-O) mutation disrupts leaf development at the ligular region of the leaf midrib by transforming blade to sheath. In a previous study, we showed that leaf sectors of Lg3 mutant activity are cell nonautonomous in the transverse dimension and can confer several alternative developmental fates (Fowler, Muehlbauer and Freeling (1996) Genetics 143, 489–503). In our present study we identify five Lg3 sector types in the leaf: sheath-like with displaced ligule (sheath-like), sheath-like with ectopic ligule (ectopic ligule), auricle-like, macro-hairless blade and wild-type blade. The acquisition of a specific sector fate depends on the timing of Lg3 expression. Early Lg3 expression results in adoption of the sheath-like phenotype at the ligule position (a proximal cell fate), whereas later Lg3 expression at the same position results in one of the more distal cell fates. Furthermore, sheath-like Lg3 sectors exhibit a graded continuum of phenotypes in the transformed blade region from the most proximal (sheath) to the most distal (wild-type blade), suggesting that cell fate acquisition is a gradual process. We propose a model for leaf cell fate acquisition based on a timing mechanism whereby cells of the leaf primordium progress through a maturation schedule of competency stages which eventually specify the cell types along the proximal to distal axis of the leaf. In addition, the lateral borders between Lg3 ‘on’ sectors and wild-type leaf sometimes provide evidence of no spreading of the transformed phenotype. In these cases, competency stages are inherited somatically.

Specification of cell fates at the dorsal margin of the zebrafish gastrula

Development ◽  
1996 ◽  
Vol 122 (7) ◽  
pp. 2225-2237 ◽  
Author(s):  
A.E. Melby ◽  
R.M. Warga ◽  
C.B. Kimmel
Keyword(s):  
Single Cells ◽  
Homeobox Gene ◽  
Dorsal Margin ◽  
Wild Type ◽  
Fate Map ◽  
Expression Domain ◽  
Kupffer’S Vesicle ◽  
Kupffer's Vesicle ◽  
Mapping Techniques ◽  
Early Gastrula

Using fate mapping techniques, we have analyzed development of cells of the dorsal marginal region in wild-type and mutant zebrafish. We define a domain in the early gastrula that is located just at the margin and centered on the dorsal midline, in which most cells generate clones that develop exclusively as notochord. The borders of the notochord domain are sharp at the level of single cells, and coincide almost exactly with the border of the expression domain of the homeobox gene floating head (flh; zebrafish homologue of Xnot), a gene essential for notochord development. In flh mutants, cells in the notochord domain generate clones of muscle cells. In contrast, notochord domain cells form mesenchyme in embryos mutant for no tail (ntl; zebrafish homologue of Brachyury). A minority of cells in the notochord domain in wild-type embryos develop as unrestricted mesoderm, invariably located in the tail, suggesting that early gastrula expression of flh does not restrict cellular potential to the notochord fate. The unrestricted tail mesodermal fate is also expressed by the forerunner cells, a cluster of cells located outside the blastoderm, adjacent to the notochord domain. We show that cells can leave the dorsal blastoderm to join the forerunners, suggesting that relocation between fate map domains might respecify notochord domain cells to the tail mesodermal fate. An intermediate fate of the forerunners is to form the epithelial lining of Kupffer's vesicle, a transient structure of the teleost tailbud. The forerunners appear to generate the entire structure of Kupffer's vesicle, which also develops in most flh mutants. Although forerunner cells are present in ntl mutants, Kupffer's vesicle never appears, which is correlated with the later severe disruption of tail development.

Metabolic Regulation of Hippocampal Neuronal Development and Its Inhibition After Irradiation

2021 ◽  
Vol 80 (5) ◽  
pp. 467-475
Author(s):  
Yu-Qing Li ◽  
C Shun Wong
Keyword(s):  
Cell Fate ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Neuronal Development ◽  
Adenosine Monophosphate ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Wild Type ◽  
Newborn Neuron ◽  
Negative Effect

Abstract 5′-Adenosine monophosphate-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, plays a role in cell fate determination. Whether AMPK regulates hippocampal neuronal development remains unclear. Hippocampal neurogenesis is abrogated after DNA damage. Here, we asked whether AMPK regulates adult hippocampal neurogenesis and its inhibition following irradiation. Adult Cre-lox mice deficient in AMPK in brain, and wild-type mice were used in a birth-dating study using bromodeoxyuridine to evaluate hippocampal neurogenesis. There was no evidence of AMPK or phospho-AMPK immunoreactivity in hippocampus. Increase in p-AMPK but not AMPK expression was observed in granule neurons and subgranular neuroprogenitor cells (NPCs) in the dentate gyrus within 24 hours and persisted up to 9 weeks after irradiation. AMPK deficiency in Cre-lox mice did not alter neuroblast and newborn neuron numbers but resulted in decreased newborn and proliferating NPCs. Inhibition of neurogenesis was observed after irradiation regardless of genotypes. In Cre-lox mice, there was further loss of newborn early NPCs and neuroblasts but not newborn neurons after irradiation compared with wild-type mice. These results are consistent with differential negative effect of AMPK on hippocampal neuronal development and its inhibition after irradiation.

scholarly journals cot1: A Regulator of Arabidopsis Trichome Initiation

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 565-577
Author(s):  
Daniel B Szymanski ◽  
Daniel A Klis ◽  
John C Larkin ◽  
M David Marks
Keyword(s):  
Cell Fate ◽  
Gene Dosage ◽  
Signal Transduction Pathway ◽  
Spatial Arrangement ◽  
Complex Signal ◽  
Chromosome 2 ◽  
Wild Type ◽  
Trichome Formation ◽  
In The Wild ◽  
Leaf Trichome

Abstract In Arabidopsis, the timing and spatial arrangement of trichome initiation is tightly regulated and requires the activity of the GLABROUS1 (GL1) gene. The COTYLEDON TRICHOME 1 (COT1) gene affects trichome initiation during late stages of leaf development and is described in this article. In the wild-type background, cot1 has no observable effect on trichome initiation. GL1 overexpression in wild-type plants leads to a modest number of ectopic trichomes and to a decrease in trichome number on the adaxial leaf surface. The cot1 mutation enhances GL1-overexpression-dependent ectopic trichome formation and also induces increased leaf trichome initiation. The expressivity of the cot1 phenotype is sensitive to cot1 and 35S::GL1 gene dosage, and the most severe phenotypes are observed when cot1 and 35S::GL1 are homozygous. The COT1 locus is located on chromosome 2 15.3 cM north of er. Analysis of the interaction between cot1, try, and 35S::GL1 suggests that COT1 is part of a complex signal transduction pathway that regulates GL1-dependent adoption of the trichome cell fate.

scholarly journals Increased Notch 1 Expression and Attenuated Stimulatory G Protein Coupling to Adenylyl Cyclase in Osteonectin-Null Osteoblasts

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1666-1674 ◽  
Author(s):  
Catherine B. Kessler ◽  
Anne M. Delany
Keyword(s):  
Adenylyl Cyclase ◽  
G Protein ◽  
Cell Fate ◽  
Osteoblastic Cells ◽  
Matricellular Protein ◽  
Wild Type ◽  
Notch 1 ◽  
Matrix Assembly ◽  
G Protein Coupling ◽  
Protein Coupling

Osteonectin, or secreted protein acidic and rich in cysteine, is one of the most abundant noncollagen matrix components in bone. This matricellular protein regulates extracellular matrix assembly and maturation in addition to modulating cell behavior. Mice lacking osteonectin develop severe low-turnover osteopenia, and in vitro studies of osteonectin-null osteoblastic cells showed that osteonectin supports osteoblast formation, maturation, and survival. The present studies demonstrate that osteonectin-null osteoblastic cells have increased expression of Notch 1, a well-documented regulator of cell fate in multiple systems. Furthermore, osteonectin-null cells are more plastic and less committed to osteoblastic differentiation, able to pursue adipogenic differentiation given the appropriate signals. Notch 1 transcripts are down-regulated by inducers of cAMP in both wild-type and osteonectin-null osteoblasts, suggesting that the mutant osteoblasts may have a defect in generation of cAMP in response to stimuli. Indeed, many bone anabolic agents signal through increased cAMP. Wild-type and osteonectin-null osteoblasts generated comparable amounts of cAMP in response to forskolin, a direct stimulator of adenylyl cyclase. However, the ability of osteonectin-null osteoblasts to generate cAMP in response to cholera toxin, a direct stimulator of Gs, was attenuated. These data imply that osteonectin-null osteoblasts have decreased coupling of Gs to adenylyl cyclase. Because osteonectin promotes G protein coupling to an effector, our studies support the concept that low-turnover osteopenia can result from reducing G protein coupled receptor activity.

scholarly journals Functional Promiscuity of Gene Regulation by Serpentine Receptors in Dictyostelium discoideum

1998 ◽  
Vol 18 (10) ◽  
pp. 5744-5749 ◽  
Author(s):  
Irene Verkerke-Van Wijk ◽  
Ji-Yun Kim ◽  
Raymond Brandt ◽  
Peter N. Devreotes ◽  
Pauline Schaap
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Dictyostelium Discoideum ◽  
Developmental Regulation ◽  
Mutant Cell ◽  
Gene Induction ◽  
Specific Gene ◽  
Wild Type ◽  
Animal Development ◽  
Camp Stimulation

ABSTRACT Serpentine receptors such as smoothened and frizzled play important roles in cell fate determination during animal development. InDictyostelium discoideum, four serpentine cyclic AMP (cAMP) receptors (cARs) regulate expression of multiple classes of developmental genes. To understand their function, it is essential to know whether each cAR is coupled to a specific gene regulatory pathway or whether specificity results from the different developmental regulation of individual cARs. To distinguish between these possibilities, we measured gene induction in car1 car3 double mutant cell lines that express equal levels of either cAR1, cAR2, or cAR3 under a constitutive promoter. We found that all cARs efficiently mediate both aggregative gene induction by cAMP pulses and induction of postaggregative and prespore genes by persistent cAMP stimulation. Two exceptions to this functional promiscuity were observed. (i) Only cAR1 can mediate adenosine inhibition of cAMP-induced prespore gene expression, a phenomenon that was found earlier in wild-type cells. cAR1’s mediation of adenosine inhibition suggests that cAR1 normally mediates prespore gene induction. (ii) Only cAR2 allows entry into the prestalk pathway. Prestalk gene expression is induced by differentiation-inducing factor (DIF) but only after cells have been prestimulated with cAMP. We found that DIF-induced prestalk gene expression is 10 times higher in constitutive cAR2 expressors than in constitutive cAR1 or cAR3 expressors (which still have endogenous cAR2), suggesting that cAR2 mediates induction of DIF competence. Since in wild-type slugs cAR2 is expressed only in anterior cells, this could explain the so far puzzling observations that prestalk cells differentiate at the anterior region but that DIF levels are actually higher at the posterior region. After the initial induction of DIF competence, cAMP becomes a repressor of prestalk gene expression. This function can again be mediated by cAR1, cAR2, and cAR3.

A developmental pathway controlling outgrowth of the Xenopus tail bud

Development ◽  
1999 ◽  
Vol 126 (8) ◽  
pp. 1611-1620 ◽  
Author(s):  
C.W. Beck ◽  
J.M. Slack
Keyword(s):  
Normal Development ◽  
Posterior Part ◽  
Neural Plate ◽  
General Mechanism ◽  
Developmental Pathway ◽  
Tail Bud ◽  
Neural Tubes ◽  
Tailbud Stage ◽  
Tail Tip ◽  
Host Embryo

We have developed a new assay to identify factors promoting formation and outgrowth of the tail bud. A piece of animal cap filled with the test mRNAs is grafted into the posterior region of the neural plate of a host embryo. With this assay we show that expression of a constitutively active Notch (Notch ICD) in the posterior neural plate is sufficient to produce an ectopic tail consisting of neural tube and fin. The ectopic tails express the evenskipped homologue Xhox3, a marker for the distal tail tip. Xhox3 will also induce formation of an ectopic tail in our assay. We show that an antimorphic version of Xhox3, Xhox3VP16, will prevent tail formation by Notch ICD, showing that Xhox3 is downstream of Notch signalling. An inducible version of this reagent, Xhox3VP16GR, specifically blocks tail formation when induced in tailbud stage embryos, comfirming the importance of Xhox3 for tail bud outgrowth in normal development. Grafts containing Notch ICD will only form tails if placed in the posterior part of the neural plate. However, if Xwnt3a is also present in the grafts they can form tails at any anteroposterior level. Since Xwnt3a expression is localised appropriately in the posterior at the time of tail bud formation it is likely to be responsible for restricting tail forming competence to the posterior neural plate in our assay. Combined expression of Xwnt3a and active Notch in animal cap explants is sufficient to induce Xhox3, provoke elongation and form neural tubes. Conservation of gene expression in the tail bud of other vertebrates suggests that this pathway may describe a general mechanism controlling tail outgrowth and secondary neurulation.

Sign in / Sign up

Export Citation Format

Share Document