bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of Xenopus embryo mesoderm-specific gene expression and dorsoanterior patterning by receptors that activate the phosphatidylinositol cycle signal transduction pathway
Authors: Ault Katherine T. , Durmowicz Gerard , Galione Antony , Harger Patricia L. , Busa William B. 
Published: April 2021

ABSTRACT
A role for the phosphatidylinositol (PI) cycle signal transduction pathway in Xenopus mesoderm induction has been revealed by observations of PI cycle activation coincident with this process, combined with the demonstration that Li+ (a PI cycle inhibitor) blocks this response and hyperdorsalizes mesoderm induction in intact embryos or augments growth factor-mediated induction in animal caps. It has been suggested that spatially restricted PI cycle activity in the marginal zone might modulate (but not, itself, activate) mesoderm induction. To better characterize the ability of PI cycle activity to modulate the pattern of mesoderm-specific gene expression elicited by mesoderm-inducing growth factors we have expressed in the embryo exogenous 5-hydroxytryptamine receptors that activate the PI cycle. In embryos, ventral expression and activation of these receptors during mesoderm induction are without obvious effect, whereas dorsal expression and activation yield dorsoanterior-deficient tadpoles. In animal caps induced with activin, simultaneous activation of exogenous 5-hydroxytryptamine receptors inhibits both convergent extension movements associated with dorsal mesoderm induction and the expression of goosecoid, a dorsal-specific gene, but is without effect on expression of a generic mesodermal marker, Xbra. All of these effects of a PI cycle-stimulating receptor are the opposites of those previously reported for the PI cycle inhibitor, Li+. PI cycle activity thus proves able to modulate the dorsal/ventral character of early mesodermal gene expression elicited by growth factor, suggesting a model for mesodermal patterning.
A novel regulatory mutation in the C. elegans sex determination gene tra-2 defines a candidate ligand/receptor interaction site
Authors: Kuwabara Patricia E. 
Published: April 2021

ABSTRACT
Sex determination in the nematode C. elegans is dependent on cell-to-cell communication, which appears to be mediated by the predicted membrane protein TRA-2A and the secreted protein HER-1. In XO males, HER-1 is hypothesised to function as a repressive ligand that inactivates the TRA-2A receptor. In XX animals, HER-1 is absent and TRA-2A promotes hermaphrodite development by negatively regulating the FEM proteins. This paper describes the molecular and genetic characterisation of a novel class of feminising mutations called tra-2(eg), for enhanced gain-of-function. In XX animals, mutant tra2(eg) activity promotes entirely normal hermaphrodite development. However, the tra-2(eg) mutations generate an XO-specific gain-of-function phenotype, because they transform XO mutants from male into hermaphrodite.
Therefore, the tra-2(eg) mutations identify a major regulatory site, which may be the TRA-2A/HER-1 interaction site. All ten tra-2(eg) mutations encode identical missense changes in a predicted extracellular domain of TRA-2A, named the EG site. It is proposed that the tra-2(eg) mutation encodes a TRA-2A protein that functions constitutively in XO animals, because it is defective in HER-1 binding. Phenotypic characterisation of sexually transformed XO tra-2(eg) hermaphrodites reveals that their fertility is strongly affected by dosage compensation mutations, suggesting that dosage compensation plays a role in normal gametogenesis.
The vegetal determinants required for the Spemann organizer move equatorially during the first cell cycle
Authors: Sakai Masao 
Published: April 2021

ABSTRACT
Embryos with no dorsal axis were obtained when more than 15% of the egg surface was deleted from the vegetal pole of the early 1-cell embryo of Xenopus laevis. The timing of the deletion in the first cell cycle was critical: dorsal-deficient embryos were obtained when the deletion began before time 0.5 (50% of the first cell cycle) whereas normal dorsal axis usually formed when the deletion was done later than time 0.8. The axis deficiency could be restored by lithium treatment and the injection of vegetal but not animal cytoplasm. Bisection of the embryo at the 2-cell stage, which is known to restore the dorsal structures in the UV-ventralized embryos, had no effect on the vegetal-deleted embryos. These results show clearly that, in Xenopus, (1) the dorsal determinants (DDs) localized in the vegetal pole region at the onset of development are necessary for dorsal axis development and (2) the DDs move from the vegetal pole to a subequatorial region where they are incorporated into gastrulating cells to form the future organizing center. A model for the early axis formation process in Xenopus is proposed.
Long-term in vitro culture and characterisation of avian embryonic stem cells with multiple morphogenetic potentialities
Authors: Pain B. , Clark M. E. , Shen M. , Nakazawa H. , Sakurai M. , Samarut J. , Etches R. J. 
Published: April 2021

ABSTRACT
Petitte, J. N., Clarck, M. E., Verrinder Gibbins, A. M. and R. J. Etches (1990; Development 108, 185-189) demonstrated that chicken early blastoderm contains cells able to contribute to both somatic and germinal tissue when injected into a recipient embryo. However, these cells were neither identified nor maintained in vitro. Here, we show that chicken early blastoderm contains cells characterised as putative avian embryonic stem (ES) cells that can be maintained in vitro for long-term culture. These cells exhibit features similar to those of murine ES cells such as typical morphology, strong reactivity toward specific anti bodies, cytokine-dependent extended proliferation and high telomerase activity. These cells also present high capacities to differentiate in vitro into various cell types including cells from ectodermic, mesodermic and endodermic lineages. Production of chimeras after injection of the cultivated cells reinforced the view that our culture system maintains in vitro some avian putative ES cells.
The germ line regulates somatic cyst cell proliferation and fate during Drosophila spermatogenesis
Authors: Gönczy Pierre , DiNardo Stephen 
Published: April 2021

ABSTRACT
Spermatogenesis relies on the function of germ-line stem cells, as a continuous supply of differentiated spermatids is produced throughout life. In Drosophila, there must also be somatic stem cells that produce the cyst cells that accompany germ cells throughout spermatogenesis. By lineage tracing, we demonstrate the existence of such somatic stem cells and confirm that of germ-line stem cells. The somatic stem cells likely correspond to the ultrastructurally described cyst progenitor cells. The stem cells for both the germ-line and cyst lineage are anchored around the hub of non-dividing somatic cells located at the testis tip. We then address whether germ cells regulate the behavior of somatic hub cells, cyst progenitors and their daughter cyst cells by analyzing cell proliferation and fate in testes in which the germ line has been genetically ablated. Daughter cyst cells, which normally withdraw from the cell cycle, continue to proliferate in the absence of germ cells. In addition, cells from the cyst lineage switch to the hub cell fate. Male-sterile alleles of chickadee and diaphanous, which are deficient in germ cells, exhibit similar cyst cell phenotypes. We conclude that signaling from germ cells regulates the proliferation and fate of cells in the somatic cyst lineage.
Oligodendrocytes and their precursors require phosphatidylinositol 3-kinase signaling for survival
Authors: Vemuri Geeta S. , McMorris F. Arthur 
Published: April 2021

ABSTRACT
Signal transduction in response to several growth factors that regulate oligodendrocyte development and survival involves the activation of phosphatidylinositol 3-kinase, which we detect in oligodendrocytes and their precursors. To investigate the role of this enzyme activity, we analyzed cell survival in cultures of oligodendrocytes treated with wortmannin or LY294002, two potent inhibitors of phosphatidylinositol 3-kinase. Cell survival was inhibited by 6070% in these cultures within 24 hours, as quantitated by a tetrazolium staining assay for viable cells and by measurement of DNA content. Similar results were obtained with oligodendrocyte precursor cells. Nuclei of the dying cells contained fragmented DNA, as revealed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assays, indicating that the cells were dying by apoptosis. Moreover, a significant increase in the number of cells with fragmented nuclear DNA was detected as early as 4 hours, well before any significant differences could be detected in glucose transport or cell viability. Exogenous addition of insulin-like growth factor-I, neurotrophin-3, platelet-derived growth factor, basic fibroblast growth factor, ciliary neurotrophic factor, N-acetyl cysteine, vitamin C, vitamin E, progesterone or serum did not prevent cell death in the presence of wortmannin or LY294002. These findings indicate that survival of oligodendrocytes and their precursors depends on a phosphatidylinositol 3-kinase mediated signaling pathway. Inhibition of this critical enzyme activity induces apoptotic cell death, even in the presence of exogenous growth factors or serum.
Abbreviations used in this paper: bFGF, basic fibroblast growth factor; CNP, 2′,3′-cyclic nucleotide 3′-phosphohydrolase; CNTF, ciliary neurotrophic factor; DMSO, dimethyl sulfoxide; EGF, epidermal growth factor; EGTA, ethylene glycol-bis(β-aminoethyl ether) N,N,N′,N′-tetraacetic acid; GC, galactocerebroside; HEPES, N-2Hydroxyethylpiperazine-N′-2-ethanesulphonic acid; IGF-I and II, insulin-like growth factor-I and II; IRS-1 and 2, insulin receptor substrate 1 and 2; MAP kinase, mitogen activated protein kinase; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NAC, N-acetyl cysteine; NT-3, neurotrophin-3; OM-5 and -6, oligodendroglial cell medium-5 and -6; PBS, phosphate buffered saline; PDGF, platelet-derived growth factor; PI(3)P, phosphatidylinositol(3)phosphate; PI(3,4)P2, phosphatidylinositol(3,4)bisphosphate; PI(3,4,5)P3, phosphatidylinositol(3,4,5)trisphosphate; PI(4)P, phosphatidylinositol(4)phosphate; PI, phosphatidylinositol; PI3-K, phosphatidylinositol 3-kinase; TCA, trichloroacetic acid; TLC, thin layer chromatography; TNF-α, tumor necrosis factor-α; TUNEL, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end-labeling assay.
A spinal cord fate map in the avian embryo: while regressing, Hensen’s node lays down the notochord and floor plate thus joining the spinal cord lateral walls
Authors: Catala Martin , Teillet Marie-Aimée , Robertis Edward M. De , Douarin Nicole M. Le 
Published: April 2021

ABSTRACT
The spinal cord of thoracic, lumbar and caudal levels is derived from a region designated as the sinus rhomboidalis in the 6-somite-stage embryo. Using quail/chick grafts performed in ovo, we show the following. (1) The floor plate and notochord derive from a common population of cells, located in Hensen’s node, which is equivalent to the chordoneural hinge (CNH) as it was defined at the tail bud stage. (2) The lateral walls and the roof of the neural tube originate caudally and laterally to Hensen’s node, during the regression of which the basal plate anlage is bisected by floor plate tissue. (3) Primary and secondary neurulations involve similar morphogenetic movements but, in contrast to primary neurulation, extensive bilateral cell mixing is observed on the dorsal side of the region of secondary neurulation. (4) The posterior midline of the sinus rhomboidalis gives rise to somitic mesoderm and not to spinal cord. Moreover, mesodermal progenitors are spatially arranged along the rest of the primitive streak, more caudal cells giving rise to more lateral embryonic structures. Together with the results reported in our study of tail bud development (Catala, M., Teillet, M.-A. and Le Douarin, N.M. (1995). Mech. Dev. 51, 51-65), these results show that the mechanisms that preside at axial elongation from the 6-somite stage onwards are fundamentally similar during the complete process of neurulation.
SHORT INTEGUMENT (SIN1), a gene required for ovule development in Arabidopsis, also controls flowering time
Authors: Ray Animesh , Lang Jean D. , Golden Teresa , Ray Sumita 
Published: April 2021

ABSTRACT
The short integument (sin1) mutation causes a femalespecific infertility, and a defect in the control of time to flowering in Arabidopsis. Female sterility of Sin− plants is due to abnormal ovule integument development and aberrant differentiation of the megagametophyte in a subset of ovules. An additional defect of sin1 mutants is the production of an increased number of vegetative leaf and inflorescence primordia leading to delayed flowering. The delayed flowering phenotype of sin1-1 is not due to a defect in the perception of day length periodicity or in gibberellic acid metabolism. Phenotypes of double mutant combina- tions of sin1 with terminal flower (tfl1) indicate that SIN1 activity is required for precocious floral induction typical in a tfl1 mutant. Unexpectedly, sin1-1 tfl1-1 plants do not make pollen, thus revealing a novel role for TFL1 in the anther. Early flowers of sin1-1 ap1-1 double mutants are transformed to long inflorescence-like shoots. A genetic model for the role of SIN1 in flowering time control is proposed.
Mutations affecting the development of the embryonic zebrafish brain
Authors: Schier Alexander F. , Neuhauss Stephan C. F. , Harvey Michele , Malicki Jarema , Solnica-Krezel Lilianna , Stainier Didier Y. R. , Zwartkruis Fried , Abdelilah Salim , Stemple Derek L. , Rangini Zehava , Yang Hong , Driever Wolfgang 
Published: April 2021

ABSTRACT
In a large scale mutagenesis screen for embryonic mutants in zebrafish, we have identified 63 mutations in 24 loci affecting the morphogenesis of the zebrafish brain. The expression of marker genes and the integrity of the axonal scaffold have been studied to investigate abnormalities in regionalization, neurogenesis and axonogenesis in the brain. Mutants can be broadly classified into two groups, one affecting regionalization along the anterior-posterior or dorsal-ventral axis, and the other affecting general features of brain morphology. The first group includes one locus that is required to generate the anlage of the midbrain-hindbrain boundary region at the beginning of somitogenesis. Four loci were identified that affect dorsalventral patterning of the brain, including the previously described cyclops locus. Mutant embryos of this class show a reduction of ventral neuroectodermal structures and variable fusion of the eyes. The second group includes a large class of mutations affecting the formation of brain ventricles. Analysis of this class reveals the requirement of a functional cardiovascular system for ventricle enlargement during embryogenesis. Mutations in one locus lead to the formation of supernumerary primary neurons, a phenotype reminiscent of neurogenic mutants in Drosophila. Other mutant phenotypes described here range from abnormalities in the fasciculation and outgrowth of axons to defects in the diameter of the neural tube. The identified loci establish the genetic foundation for a further analysis of the development of the zebrafish embryonic brain.
Mutations in zebrafish genes affecting the formation of the boundary between midbrain and hindbrain
Authors: Brand Michael , Heisenberg Carl-Philipp , Jiang Yun-Jin , Beuchle Dirk , Lun Klaus , Furutani-Seiki Makoto , Granato Michael , Haffter Pascal , Hammerschmidt Matthias , Kane Donald A. , Kelsh, Robert N. , Mullins Mary C. , Odenthal Jörg , Eeden Fredericus J. M. van , Nüsslein-Volhard Christiane 
Published: April 2021

ABSTRACT
Mutations in two genes affect the formation of the boundary between midbrain and hindbrain (MHB): no isthmus (noi) and acerebellar (ace). noi mutant embryos lack the MHB constriction, the cerebellum and optic tectum, as well as the pronephric duct. Analysis of noi mutant embryos with neuron-specific antibodies shows that the MHB region and the dorsal and ventral midbrain are absent or abnormal, but that the rostral hindbrain is unaffected with the exception of the cerebellum. Using markers that are expressed during its formation (eng, wnt1 and pax-b), we find that the MHB region is already misspecified in noi mutant embryos during late gastrulation. The tectum is initially present and later degenerates. The defect in ace mutant embryos is more restricted: MHB and cerebellum are absent, but a tectum is formed. Molecular organisation of the tectum and tegmentum is disturbed, however, since eng, wnt1 and pax-b marker gene expression is not maintained. We propose that noi and ace are required for development of the MHB region and of the adjacent mid- and hindbrain, which are thought to be patterned by the MHB region.
Presence of pax-b RNA, and absence of pax-b protein, together with the observation of genetic linkage and the occurrence of a point mutation, show that noi mutations are located in the pax-b gene. pax-b is a vertebrate orthologue of the Drosophila gene paired, which is involved in a pathway of cellular interactions at the posterior compartment boundary in Drosophila. Our results confirm and extend a previous report, and show that at least one member of this conserved signalling pathway is required for formation of the boundary between midbrain and hindbrain in the zebrafish.
Genetic analysis of fin formation in the zebrafish, Danio rerio
Authors: van Eeden Fredericus J. M. , Granato Michael , Schach Ursula , Brand Michael , Furutani-Seiki Makoto , Haffter Pascal , Hammerschmidt Matthias , Heisenberg Carl-Philipp , Jiang Yun-Jin , Kane Donald A. , Kelsh Robert N. , Mullins Mary C. , Odenthal Jörg , Warga Rachel M. , Nüsslein-Volhard Christiane 
Published: April 2021

ABSTRACT
In the zebrafish, Danio rerio, a caudal and pectoral fin fold develop during embryogenesis. At larval stages the caudal fin fold is replaced by four different fins, the unpaired anal, dorsal and tail fins. In addition the paired pelvic fins are formed. We have identified a total of 118 mutations affecting larval fin formation. Mutations in 11 genes lead to abnormal morphology or degeneration of both caudal and pectoral fin folds. Most mutants survive to adulthood and form a surprisingly normal complement of adult fins.
Mutations in nine genes result in an increased or reduced size of the pectoral fins. Interestingly, in mutants of one of these genes, dackel (dak), pectoral fin buds form initially, but later the fin epithelium fails to expand. Expression of sonic hedgehog mRNA in the posterior mesenchyme of the pectoral fin bud is initiated in dak embryos, but not maintained.
Mutations in five other genes affect adult fin but not larval fin development. Two mutants, longfin (lof) and another longfin (alf) have generally longer fins. Stein und bein (sub) has reduced dorsal and pelvic fins, whereas finless (fls) and wanda (wan) mutants affect all adult fins. Finally, mutations in four genes causing defects in embryonic skin formation will be briefly reported.
Mutations affecting the formation and function of the cardiovascular system in the zebrafish embryo
Authors: Stainier Didier Y. R. , Fouquet Bernadette , Chen Jau-Nian , Warren Kerri S. , Weinstein Brant M. , Meiler Steffen E. , Mohideen Manzoor-Ali P. K. , Neuhauss Stephan C. F. , Solnica-Krezel Liliana , Schier Alexander F. , Zwartkruis Fried , Stemple Derek L. , Malicki Jarema , Driever Wolfgang , Fishman Mark C. 
Published: April 2021

ABSTRACT
As part of a large-scale mutagenesis screen of the zebrafish genome, we have identified 58 mutations that affect the formation and function of the cardiovascular system. The cardiovascular system is particularly amenable for screening in the transparent zebrafish embryo because the heart and blood vessels are prominent and their function easily examined. We have classified the mutations affecting the heart into those that affect primarily either morphogenesis or function.
Nine mutations clearly disrupt the formation of the heart. cloche deletes the endocardium. In cloche mutants, the myocardial layer forms in the absence of the endocardium but is dysmorphic and exhibits a weak contractility. Two loci, miles apart and bonnie and clyde, play a critical role in the fusion of the bilateral tubular primordia. Three mutations lead to an abnormally large heart and one to the formation of a diminutive, dysmorphic heart. We have found no mutation that deletes the myocardial cells altogether, but one, pandora, appears to eliminate the ventricle selectively.
Seven mutations interfere with vascular integrity, as indicated by hemorrhage at particular sites.
In terms of cardiac function, one large group exhibits a weak beat. In this group, five loci affect both chambers and seven a specific chamber (the atrium or ventricle). For example, the weak atrium mutation exhibits an atrium that becomes silent but has a normally beating ventricle. Seven mutations affect the rhythm of the heart causing, for example, a slow rate, a fibrillating pattern or an apparent block to conduction. In several other mutants, regurgitation of blood flow from ventricle to atrium is the most prominent abnormality, due either to the absence of valves or to poor coordination between the chambers with regard to the timing of contraction.
The mutations identified in this screen point to discrete and critical steps in the formation and function of the heart and vasculature.
The zebrafish epiboly mutants
Authors: Kane Donald A. , Hammerschmidt Matthias , Mullins Mary C. , Maischein Hans-Martin , Brand Michael , van Eeden Fredericus J. M. , Furutani-Seiki Makoto , Granato Michael , Haffter Pascal , Heisenberg Carl-Philipp , Jiang Yun-Jin , Kelsh Robert N. , Odenthal Jörg , Warga Rachel M. , Nüsslein-Volhard Christiane 
Published: April 2021

ABSTRACT
Epiboly, the enveloping of the yolk cell by the blastoderm, is the first zebrafish morphogenetic movement. We isolated four mutations that affect epiboly: half baked, avalanche, lawine and weg. Homozygous mutant embryos arrest the vegetal progress of the deep cells of the blastoderm; only the yolk syncytial layer of the yolk cell and the enveloping layer of the blastoderm reach the vegetal pole of the embryo. The mutations half baked, avalanche and lawine produce a novel dominant effect, termed a zygotic-maternal dominant effect: heterozygous embryos produced from heterozygous females slow down epiboly and accumulate detached cells over the neural tube; a small fraction of these mutant individuals are viable. Heterozygous embryos produced from heterozygous males crossed to homozygous wild-type females complete epiboly normally and are completely viable. Additionally, embryos heterozygous for half baked have an enlarged hatching gland, a partial dominant phenotype. The phenotypes of these mutants demonstrate that, for the spreading of cells during epiboly, the movement of the deep cells of the blastoderm require the function of genes that are not necessary for the movement of the enveloping layer or the yolk cell. Furthermore, the dominant zygotic-maternal effect phenotypes illustrate the maternal and zygotic interplay of genes that orchestrate the early cell movements of the zebrafish.