bluuebunny/crossref_metadata_2025_split huggingface dataset:
Xwnt-8b: a maternally expressed Xenopus Wnt gene with a potential role in establishing the dorsoventral axis
Authors: Cui Yanzhen , Brown Jeffrey D. , Moon Randall T. , Christian Jan L. 
Published: April 2021

ABSTRACT
In amphibian embryos, establishment of dorsal-ventral asymmetry is believed to involve dorsal-ventral differences in vegetally derived mesoderm-inducing signals and/or differences in the competence of animal hemisphere (ectodermal) cells to respond to these signals. Previous studies have shown that certain Wnt proteins can generate an ectopic dorsal axis when misexpressed, and that they do so by modifying the response of ectodermal cells to inducers. None of these Wnt proteins are expressed at an appropriate time to do so in vivo. In this study, we describe the isolation and characterization of a full length cDNA for the Xenopus Wnt gene, Xwnt-8b, whose biological activity and expression pattern suggest that it may be involved in establishment of the dorsoventral axis. Both maternal and zygotic Xwnt-8b transcripts undergo alternative splicing to generate mRNAs which encode two different forms of Xwnt-8b protein. During early cleavage stages Xwnt-8b transcripts are confined primarily to animal hemisphere blastomeres, while zygotically derived Xwnt-8b transcripts are restricted almost exclusively to a band of cells in the prospective forebrain of neurula and tailbud stage embryos. Ectopically expressed Xwnt-8b can completely rescue dorsal development of embryos ventralized by exposure to ultraviolet light, and can induce a complete secondary axis in wild-type embryos. Axis induction is observed only if Xwnt-8b is supplied prior to the onset of zygotic gene transcription. This biological activity, together with the presence of maternal Xwnt-8b transcripts in cells that will be induced to form the dorsal mesoderm, is consistent with the possibility that Xwnt-8b may be the endogenous agent that establishes asymmetry in the response of ectodermal cells to mesoderm-inducing signals, thereby initiating dorsal development.
Induction of prostatic morphology and secretion in urothelium by seminal vesicle mesenchyme
Authors: Donjacour Annemarie A. , Cunha Gerald R. 
Published: April 2021

ABSTRACT
Mesenchymal-epithelial interactions are essential for the development of the male reproductive tract. Tissue recombination experiments have been used to define the characteristics of these interactions. When mesenchyme, embryonic connective tissue, is recombined with epithelium from another organ an instructive induction may occur in which the developmental fate of the epithelium is altered. Instructive inductions are most common when the epithelium that is removed from the mesenchyme and the epithelium that is recombined with the mesenchyme are from the same germ layer. All of the mesenchyme of the male reproductive tract is of mesodermal origin. The epithelia of these organs are derived from either the mesodermal Wolffian duct epithelium or the endodermal urogenital sinus epithelium. Urogenital sinus mesenchyme can instructively induce bladder and urethral epithelium to form prostate (Donjacour, A. A. and Cunha, G. R. (1993) Endocrinol. 132, 2342-2350) and seminal vesicle mesenchyme can instructively induce epithelium from the ductus deferens and ureter (Cunha, G. R., Young, P., Higgins, S. J. and Cooke, P. S. (1991) Development 111, 145-158) to form seminal vesicle. To see whether inductive interactions could occur across germ layers in this system, seminal vesicle mesenchyme, normally associated with a mesodermal epithelium, was recombined with epithelium from neonatal or adult bladder or urethra, which are of endodermal origin. The resulting tissue recombinants were analyzed histologically and by immunocytochemistry and western blotting with antibodies to prostatic and seminal vesicle secretory proteins. Full prostatic differentiation was observed in tissue recombinants made with seminal vesicle mesenchyme plus either adult or neonatal bladder or urethral epithelium. These tissue recombinants made dorsolateral but not ventral prostatic secretory proteins. None of them developed into seminal vesicle. To examine whether epithelial androgen receptors were required for this process, seminal vesicle mesenchyme was recombined with urothelium from mice with the testicular feminization mutation. These mice lack functional androgen receptors. While these tissue recombinants grew, no prostatic proteins were detected. Seminal vesicle mesenchyme acted as a potent prostatic inducer, indicating that similar mesenchymal signals can induce prostatic and seminal vesicle development. Urogenital epithelia of both endodermal and mesodermal origin appeared to be able to respond to these inductive signals produced by the seminal vesicle mesenchyme; however, their responses differed depending on their germ layer of origin: mesodermal epithelium yielding seminal vesicle (Cunha, G. R., Young, P., Higgins, S. J. and Cooke, P. S. (1991) Development 111, 145-158) and endodermal epithelium yielding prostate.
Regulation of mouse egg activation: presence of ryanodine receptors and effects of microinjected ryanodine and cyclic ADP ribose on uninseminated and inseminated eggs
Authors: Ayabe Takuya , Kopf Gregory S. , Schultz Richard M. 
Published: April 2021

ABSTRACT
Sperm-induced activation of mammalian eggs is associated with a transient increase in Ca2+ concentrations thought to be derived from inositol 1,4,5-trisphosphate-sensitive and -insensitive intracellular stores. Whereas the importance of inositol 1,4,5-trisphosphate-sensitive Ca2+ stores has been evaluated, the identity and role of inositol 1,4,5-trisphos- phate-insensitive stores are poorly understood. To explore the role of the ryanodine-sensitive Ca2+ store, we first used reverse transcription-polymerase chain reaction to identify transcripts of the ryanodine receptor in eggs and deter- mined that transcripts for the type 2 and 3 receptor were present. Immunoprecipitation of radioiodinated egg extracts with an antibody that recognizes both type 2 and 3 receptors detected specifically a band of Mr=520,000. Immunolocalization of the receptor(s) using laser-scanning confocal microscopy revealed that the receptor(s) was uniformly distributed in the cortex of the germinal vesicle- intact oocyte, but became asymmetrically localized to the cortex in a region apposed to the meiotic spindle in the metaphase II-arrested egg; this asymmetrical localization developed by metaphase I. The role of the ryanodine receptor in mouse egg activation was examined by deter- mining the effects of microinjected ryanodine or cyclic ADP ribose on endpoints of egg activation in either unin- seminated or inseminated eggs. Ryanodine induced the conversion of the zona pellucida glycoprotein ZP2 to its postfertilization form ZP2f in a biphasic concentration- dependent manner; nanomolar concentrations stimulated this conversion, whereas micromolar concentrations had no stimulatory effect. Cyclic ADP ribose also promoted the ZP2 conversion, but with a hyperbolic concentration dependence. Neither of these compounds induced cell cycle resumption. Inhibiting the inositol 1,4,5-trisphosphate- sensitive Ca2+ store did not inhibit the ryanodine-induced ZP2 conversion and, reciprocally, inhibiting the ryanodine- sensitive Ca2+ store did not inhibit the inositol 1,4,5- trisphosphate-induced ZP2 conversion. Last, treatment of eggs under conditions that would block the release of Ca2+ from the ryanodine-sensitive store had no effect on any event of egg activation following fertilization. Results of these experiments suggest that although ryanodine receptors are present and functional, release of Ca2+ from this store is not essential for sperm-induced egg activation.
Distinct expression and shared activities of members of the hedgehog gene family of Xenopus laevis
Authors: Ekker Stephen C. , Lynn McGrew L. , Lai Cheng-Jung , Lee John J. , von Kessler Doris P. , Moon Randall T. , Beachy Philip A. 
Published: April 2021

ABSTRACT
The hedgehog family of signaling proteins is associated with a variety of spatial patterning activities in insects and vertebrates. Here we show that new members of this family isolated from Xenopus laevis are expressed embryonically in patterns suggestive of roles in patterning in the ectoderm, nervous system and somites. Banded hedgehog is expressed throughout the neural plate and subsequently in both the nervous system and in the dermatome of somites. Cephalic hedgehog is expressed in anterior ectoderm and endodermal structures, and sonic hedgehog is expressed in patterns which parallel those in other species. Injection of RNAs encoding Xenopus hedgehogs induces ectopic cement gland formation in embryos. Similar to reported activities of noggin and follistatin, Xenopus hedgehogs share a common ability to induce cement glands in animal cap explants. However, hedgehog activities in naive ectoderm appear capable of acting independently of noggin and fol-listatin since, although all three are induced by activin in animal cap explants, X-hh expression does not induce noggin or follistatin.
Isolation of novel tissue-specific genes from cDNA libraries representing the individual tissue constituents of the gastrulating mouse embryo
Authors: Harrison S. M. , Dunwoodie S. L. , Arkell R. M. , Lehrach H. , Beddington R. S. P. 
Published: April 2021

ABSTRACT
A total of 5 conventional, directionally cloned plasmid cDNA libraries have been constructed from the entire embryonic region of the mid-gastrulation mouse embryo and from its four principal tissue constituents (ectoderm, mesoderm, endoderm and primitive streak). These libraries have been validated with respect to the number of independent clones, insert-size and appropriate representation of diagnostic marker genes. Subtractive hybridisation has been used to remove clones common to the Endoderm and Mesoderm cDNA libraries resulting in an Endoderm minus Mesoderm subtracted library. Probe prepared from this subtracted library has been hybridised to a grid containing approximately 18,500 Embryonic Region library clones. Three novel clones have been recovered as well as expected genes already known to be highly expressed in the primitive endoderm lineage at this stage of development. In situ hybridisation to early postim-plantation embryos has revealed the expression patterns of these novel genes. One is highly expressed exclusively in visceral endoderm, one is expressed in ectodermal and endodermal tissues, and the third proves to be an early marker of prospective and differentiated surface ectoderm as well as being expressed in endoderm and its derivatives.
Epithelial-mesenchymal conversion of dermatome progenitors requires neural tube-derived signals: characterization of the role of Neurotrophin-3
Authors: Brill Gilat , Kahane Nitza , Carmeli Chana , von Schack David , Barde Yves-Alain , Kalcheim Chaya 
Published: April 2021

ABSTRACT
Development of the somite-derived dermatome involves conversion of the epithelial dermatome progenitors into mesenchymal cells of the dermis. In chick embryos, neural tube-derived signals are required for this conversion, as the interposition of a membrane between neural tube and somites results in a failure of the dermatome to lose its epithelial arrangement. However, dermis formation can be completely rescued by coating the membranes with Neurotrophin-3, but not with the related molecule Nerve growth factor. Neurotrophin-3 was also found to be necessary for dermatome dissociation using in vitro explants or partially dissociated dermomyotomes. The functional relevance of these observations was investigated by neutralizing endogenous Neurotrophin-3 using a specific blocking antibody. Antibody-treated embryos revealed the presence of tightly aggregated cells between myotome and ectoderm instead of the loose dermal mesenchyme observed in embryos treated with control antibodies. As previous studies have demonstrated the presence of Neurotrophin-3 in the neural tube, these results suggest that it may be a necessary neural tube-derived signal required for early stages of dermis formation.
Fusion from myoblasts to myotubes is dependent on the rolling stone gene (rost) of Drosophila
Authors: Paululat Achim , Burchard Susanne , Renkawitz-Pohl Renate 
Published: April 2021

ABSTRACT
The development and differentiation of the body wall musculature in Drosophila are accompanied by changes in gene expression and cellular architecture. We isolated a Drosophila gene, termed rolling stone (rost), which, when mutated, specifically blocks the fusion of mononucleated cells to myotubes in the body wall musculature. β3 tubulin, which is an early marker for the onset of mesoderm differentiation, is still expressed in these cells. Gastrulation and mesoderm formation, as well as the development of the epidermis and of the central and peripheral nervous systems, appear quite normal in homozygous rolling stone embryos. Embryonic development stops shortly before hatching in a P-element-induced mutant, as well as in 16 EMS-induced alleles. In mutant embryos, other mesodermal derivatives such as the visceral mesoderm and the dorsal vessel, develop fairly normally and defects are restricted to the body wall musculature. Myoblasts remain as single mononucleated cells, which express muscle myosin, showing that the developmental program of gene expression proceeds. These myoblasts occur at positions corresponding to the locations of dorsal, ventral and pleural muscles, showing that the gene rolling stone is involved in cell fusion, a process that is independent of cell migration in these mutants. This genetic analysis has set the stage for a molecular analysis to clarify where the rolling stone action is manifested in the fusion process and thus gives insight into the complex regulating network controlling the differentiation of the body wall musculature.
Mosaic analysis of the let-23 gene function in vulval induction of Caenorhabditis elegans
Authors: Koga Makoto , Ohshima Yasumi 
Published: April 2021

ABSTRACT
The let-23 receptor tyrosine kinase gene is required for vulval induction and larval survival in the nematode Caenorhabditis elegans. We carried out genetic mosaic analyses of the let-23 gene function by using the cloned let-23 and ncl-1 genes. The wild-type let-23 gene was required in a vulval precursor cell to adopt the 1° vulval fate in animals carrying a let-23 vulvaless or lethal chromosomal mutation. In almost all the animals, vulval precursor cells adjacent to a 1° fate cell were induced to the 2° vulval fate regardless of the let-23 genotypes. These findings indicate that the vulval induction signal from an anchor cell induces a vulval precursor cell to adopt the 1° fate through LET-23, and then a 1° fate cell induces adjacent cells to adopt the 2° fate, for which LET-23 is not required. Foci of lethality of the let-23 (mn23) mutation were found in ABal and ABplp lineages.
The Hox11 gene is essential for cell survival during spleen development
Authors: Dear T. N. , Colledge W. H. , Carlton M. B. L. , Lavenir I. , Larson T. , Smith A. J. H. , Warren A. J. , Evans M. J. , Sofroniew M. V. , Rabbitts T. H. 
Published: April 2021

ABSTRACT
The HOX11 homeobox gene was identified via the translocation t(10;14) in T cell leukaemia. To determine the function of this gene in mice, null mutations were made using homologous recombination in ES cells to incorporate lacZ into the hox11 transcription unit. Production of β-galactosidase from the recombinant hox11 allele in +/− mutants allowed identification of sites of hox11 expression which included the developing spleen. Newborn hox11 −/− mice exhibit asplenia. Spleen formation commences normally at E11.5 in hox11 −/− mutant embryos but the spleen anlage undergoes rapid and complete resorption between E12.5 and E13.5. Dying spleen cells exhibit molecular features of apoptosis, suggesting that programmed cell death is initiated at this stage of organ development in the absence of hox11 protein. Thus hox11 is not required to initiate spleen development but is essential for the survival of splenic precursors during organogenesis. This function for hox11 suggests that enhanced cell survival may result from the t(10;14) which activates HOX11 in T cell leukaemias, further strengthening the association between oncogene-induced cell survival and tumorigenesis.
A role for the Drosophila Bag-of-marbles protein in the differentiation of cystoblasts from germline stem cells
Authors: McKearin Dennis , Ohlstein Benjamin 
Published: April 2021

ABSTRACT
Cell differentiation commonly dictates a change in the cell cycle of mitotic daughters. Previous investigations have suggested that the Drosophila bag of marbles (bam) gene is required for the differentiation of germline stem cell daughters (cystoblasts) from the mother stem cells, perhaps by altering the cell cycle. In this paper, we report the preparation of antibodies to the Bam protein and the use of those reagents to investigate how Bam is required for germ cell development. We find that Bam exists as both a fusome component and as cytoplasmic protein and that cytoplasmic and fusome Bam might have separable activities. We also show that bam mutant germ cells are blocked in differentiation and are trapped as mitotically active cells like stem cells. A model for how Bam might regulate cystocyte differentiation is presented.
Apoptosis in the developing tooth: association with an embryonic signaling center and suppression by EGF and FGF-4
Authors: Vaahtokari Anne , Åberg Thomas , Thesleff Irma 
Published: April 2021

ABSTRACT
Apoptosis was localized in developing mouse teeth from initiation of morphogenesis to completion of cusp formation by using modified TUNEL method for serial sections and Nile Blue staining for whole mounts. Apoptosis was first detected at bud stage (E12-E13) in the central cells of the invaginating dental epithelium suggesting involvement of cell death in epithelial budding morphogenesis. During cusp development, apoptotic cells were located in the enamel knots, which are transient clusters of dental epithelial cells proposed to act as signaling centers directing the morphogenesis of tooth cusps. Apoptosis was also detected in other restricted epithelial cell populations including the dental lamina, ameloblasts, as well as stratum intermedium and stellate reticulum cells suggesting that the removal of these epithelial cells occurs by apoptosis. Apoptotic cells, presumably osteoclasts, were also located on the surfaces of the developing alveolar bone.
When dissected E13 dental epithelium or mesenchyme were cultured in isolation, apoptotic cells were abundant throughout the tissues, whereas when cultured together, apoptosis was inhibited in both tissues close to their interface indicating that epithelial-mesenchymal tissue interactions prevent apoptosis. Epidermal growth factor (EGF) and fibroblast growth factor-4 (FGF-4) inhibited apoptosis in the dental mesenchyme when applied locally using agarose or heparin-coated acrylic beads, suggesting involvement of these or related growth factors in the prevention of apoptosis in dental tissues in vivo.
The spatially and temporally restricted distribution patterns of apoptotic cells suggest multiple roles for programmed cell death in dental development. Of particular interest is the removal of the enamel knots by apoptosis which may terminate their tasks as regulators of the patterning of the tooth cusps. The apical ectodermal ridge (AER) of the limb bud has similar signaling characteristics as the enamel knot, and it also undergoes apoptosis. Hence, apoptosis may be a general mechanism for the silencing of embryonic signaling centers.
glide directs glial fate commitment and cell fate switch between neurones and glia
Authors: Vincent Stéphane , Vonesch Jean-Luc , Giangrande Angela 
Published: April 2021

ABSTRACT
Glial cells constitute the second component of the nervous system and are important during neuronal development. In this paper we describe a gene, glial cell deficient, (glide), that is necessary for glial cell fate commitment in Drosophila melanogaster. Mutations at the glide locus prevent glial cell determination in the embryonic central and peripheral nervous system. Moreover, we show that the absence of glial cells is the consequence of a cell fate switch from glia to neurones. This suggests the existence of a multipotent precursor cells in the nervous system. glide mutants also display defects in axonal navigation, which confirms and extends previous results indicating a role for glial cells in these processes.
The eve stripe 2 enhancer employs multiple modes of transcriptional synergy
Authors: Arnosti David N. , Barolo Scott , Levine Michael , Small Stephen 
Published: April 2021

ABSTRACT
Previous studies have provided a detailed model for the regulation of even-skipped (eve) stripe 2 expression in the Drosophila embryo. The bicoid (bcd) regulatory gradient triggers the expression of hunchback (hb); these work synergistically to activate the stripe in the anterior half of the embryo. bcd also coordinates the expression of two repressors, giant (gt) and Kruppel (Kr), which define the anterior and posterior borders of the stripe, respectively. Here, we report the findings of extensive cis- and trans-complementation analyses using a series of defective stripe 2 enhancers in transgenic embryos. This study reaches two primary conclusions. First, the stripe 2 enhancer is inherently ‘sensitized’ for repression by gt. We propose that gt specifies the sharp anterior stripe border by blocking two tiers of transcriptional synergy, cooperative binding to DNA and cooperative contact of bound activators with the transcription complex. Second, we find that the synergistic activity of hb and bcd is ‘promiscuous’. For example, a maternally expressed Gal4-Sp1 fusion protein can functionally replace hb in the stripe 2 enhancer. This finding challenges previous proposals for dedicated hb and bcd interactions in the segmentation process.
In vivo effects of neurotrophin-3 during sensory neurogenesis
Authors: Ockel Michaela , Lewin Gary R. , Barde Yves-Alain 
Published: April 2021

ABSTRACT
The neurotrophins nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 are structurally related proteins regulating the number of neurons in peripheral ganglia of the nervous system. Increased levels of nerve growth factor or of brain-derived neurotrophic factor selectively prevent normally occurring neuronal death, while the targeted elimination of all three genes decreases neuronal numbers. As previous studies indicated that the lack of neurotrophin-3 affects sensory ganglia already during gangliogenesis, the levels of this neurotrophin were increased during selected periods of chick development. We found that early, but not late, applications of neurotrophin-3 lead to a marked decrease in neuronal numbers in peripheral sensory ganglia. This decrease is not seen with BDNF and does not selectively affect subtypes of dorsal root ganglion neurons. It is accompanied by, and might result from, a decrease in the number of proliferating neuroblasts in sensory ganglia of treated embryos.