bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distribution of tudor protein in the Drosophila embryo suggests separation of functions based on site of localization
Authors: Bardsley Anne , McDonald Kent , Boswell Robert E. 
Published: April 2021

ABSTRACT
Mutations in the tudor locus of Drosophila affect two distinct determinative processes in embryogenesis; segmentation of the abdomen and determination of the primordial germ cells. The distribution of tudor protein during embryogenesis, and the effect of various mutations on its distribution, suggest that tudor protein may carry out these functions separately, based on its location in the embryo. The protein is concentrated in the posterior pole cytoplasm (germ plasm), where it is found in polar granules and mitochondria. Throughout the rest of the embryo, tudor protein is associated with the cleavage nuclei. Mutations in all maternal genes known to be required for the normal functioning of the germ plasm eliminate the posterior localization of tudor protein, whereas mutations in genes required for the functioning of the abdominal determinant disrupt the localization around nuclei. Analysis of embryos of different maternal genotypes indicates that the average number of pole cells formed is correlated with the amount of tudor protein that accumulates in the germ plasm. Our results suggest that tudor protein localized in the germ plasm is instrumental in germ cell determination, whereas nuclear-associated tudor protein is involved in determination of segmental pattern in the abdomen.
Restricted expression of the hyaluronan receptor, CD44, during postimplantation mouse embryogenesis suggests key roles in tissue formation and patterning
Authors: Wheatley Susan C. , Isacke Clare M. , Crossley Philip H. 
Published: April 2021

ABSTRACT
CD44 is a multifunctional adhesion protein that acts as a major receptor for the hygroscopic extracellular matrix component, hyaluronan. This receptor-ligand binding directly mediates at least some of the cell-cell and cell-matrix interactions ascribed to CD44. Other interactions involving CD44 may be modulated indirectly by its ability to bind growth factors and thereby to promote cell attachment. During vertebrate development, multiple cases of hyaluronan involvement in cell proliferation, cell migration and histogenesis have been documented. In addition, there is evidence suggesting a central role for cell surface glycoproteins and proteoglycans in mediating the action of polypeptide growth factors involved in tissue patterning. In view of this, we undertook to investigate expression of the CD44 protein during postimplantation mouse embryogenesis. Between 9.5 and 12.5 days of embryonic development, the pre-dominant form of CD44 protein corresponds to the hyaluronan-binding CD44H form. However, species with a higher Mr were also detected, implying that CD44 isoforms generated by alternative splicing of CD44 RNA are employed in normal development. Further, we used mouse embryos to perform whole-mount immunohistochemistry and examine the temporal and spatial distribution of this glycoprotein. CD44 is expressed at high levels in the heart, somites and condensing limb-bud mesenchyme at critical stages of morphogenesis. These sites correlate with regions where hyaluronan has been demonstrated to regulate morphogenetic events. Of novel interest, however, is the high expression of CD44 in regions that do not correlate with sites of known hyaluronan-mediated developmental events. These include instructive epithelia participating in epithelial-mesenchymal cell interactions such as the apical ectodermal ridge of the developing limb bud and the odontogenic placodes of the presumptive upper and lower jaws.
Two rhombomeres are altered in Hoxa-1 mutant mice
Authors: Mark Manuel , Lufkin Thomas , Vonesch Jean-Luc , Ruberte Esther , Olivo Jean-Christophe , Dollé Pascal , Gorry Philippe , Lumsden Andrew , Chambon Pierre 
Published: April 2021

ABSTRACT
This study provides a detailed description of the anatomical defects in the Hoxa-1−/−mutant mice previously generated in our laboratory (T. Lufkin, A. Dierich, M. LeMeur, M. Mark and P. Chambon, 1991; Cell 66, 1105-1119). Three-dimensional reconstructions of the Hoxa-1−/− rhombencephalon reveals that it bears only five rhombomeric structures (ie. morphological segments) instead of the normal seven. The first three of these rhombomeres appear normal as judged from the distribution pattern of CRABPI transcripts in the neurectoderm and from the histological analysis of the cranial nerve components derived from these structures. In contrast, the neural-crest-cell-free region normally located opposite rhombomere 5 is lacking in Hoxa-1−/− embryos, and motor neurons of the facial and abducens nerves, which normally differentiate within rhombomeres 4, 5 and 6, are missing in Hoxa-1−/− fetuses. These morphological data, combined with the determination of the molecular positional identities of the rhombomeres 4 and 5 (P. Dollé, T. Lufkin, R. Krumlauf, M. Mark, D. Duboule and P. Chambon, 1993; Proc. Natl. Acad. Sci. USA, in press), suggest that rhombomere 4 is markedly reduced, whereas rhombomere 5 is almost absent. Thus, the remnants of rhombomeres 4 and 5 appear to be fused caudally with rhombomere 6 to form a single fourth rhombomeric structure. Moreover, the migration of neural crest cells contributing to the glossopharyngeal and vagus nerves occurs in a more rostral position, resulting in abnormalities of these cranial nerves, which were visualized by whole-mount anti-neurofilament immunostaining. The mutual relationship along the rostrocaudal axis between the otic pit and the neuroepithelial site of int-2 protein secretion (a putative otogenic cue) is not significantly changed in Hoxa-1−/− embryos. However, the abnormal relationship between the rhombencephalon and the epithelial inner ear may account for the aplasia and faulty differentiation of the membranous labyrinth, the disruption of the cartilaginous otic capsule and the disorganisation of some middle ear structures. This phenotype is compared with that of the Hoxa-1−/− mutants generated by O. Chisaka, T. S. Musci and M. R. Capecchi, 1992 (Nature 335, 516-520) and with that of the mice homozygous for the kreisler mutation.
Mechanisms of compartment formation: Evidence that non-proliferating cells do not play a critical role in defining the D/V lineage restriction in the developing wing of Drosophila
Authors: Blair Seth S. 
Published: April 2021

ABSTRACT
The dorsoventral (D/V) lineage boundary in the developing wing disc of Drosophila restricts growing cells to the prospective dorsal or ventral compartments of the wing blade. This restriction appears along the prospective margin of the wing some time during the middle to late stages of wing disc growth. It has been proposed that the restriction is established and maintained by the formation of a zone of non-proliferating cells that acts as a barrier between cells in the dorsal and ventral compartments (O’Brochta and Bryant, Nature 313, 138-141, 1985). In the adult, however, no group of barrier cells has been identified between the compartments. This study will show the following. (1) A group of cells does exist that lies between the dorsal and ventral rows of margin bristle precursors; these cells, which express cut in the late third instar wing disc, are thus in an ideal position to act as barrier cells. (2) This cut-expressing region is split into dorsal and ventral regions by the expression of the dorsal-specific gene apterous. (3) The D/V lineage restriction defined by marked dorsal and ventral clones lies in the middle of the cut-expressing region and is exactly congruent with the boundary of apterous expression. (4) No group of barrier cells is observed between dorsal and ventral clones. (5) Clones often run along the boundary for long distances, suggesting that they can grow along the D/V boundary without crossing it. These results thus do not support the existence of a groups of cells acting as a barrier between dorsal and ventral compartments. Nor do they support a critical role for division rates near the D/V boundary in establishing or maintaining the lineage restriction.
δ-crystallin enhancer binding protein δEF1 is a zinc finger-homeodomain protein implicated in postgastrulation embryogenesis
Authors: Funahashi Jun-ichi , Sekido Ryohei , Murai Kasumi , Kamachi Yusuke , Kondoh Hisato 
Published: April 2021

ABSTRACT
We investigated nuclear factors that bind to δ1-crystallin enhancer core and regulate lens-specific transcription. A nuclear factor δEF1, which binds to the essential element of the δ1-crystallin enhancer core, was molecularly cloned from the chicken by a southwestern method. The protein organization of δEF1 deduced from the cDNA sequence indicated that it has heterogeneous domains for DNA-binding, two widely separated zinc fingers and a homeodomain, analogous to Drosophila ZFH-1 protein. The C-terminal zinc fingers were found to be responsible for binding to the δ1-crystallin enhancer core sequence. δEF1 had proline-rich and acidic domains common to various transcriptional activators. During embryogenesis, δEF1 expression was observed in the postgastrulation period in mesodermal tissues; initially, in the notochord, followed by somites, nephrotomes and other components. The expression level changed dynamically in a tissue, possibly reflecting the differentiation states of the constituent cells. Besides mesoderm, δEF1 was expressed in the nervous system and the lens, but other ectodermal tissues and endoderm remained very low in δEF1 expression. Cotransfection experiments indicated that this factor acts as a repressor of δ1-crystallin enhancer. Possession of heterogeneous DNA-binding domains and its dynamic change of expression in embryogenesis strongly suggest that EF1 acts in multiple ways depending on the cell type and the gene under its regulation.
Relationship between expression of serendipity α and cellularisation of the Drosophila embryo as revealed by interspecific transformation
Authors: Ibnsouda Saad , Schweisguth François , de Billy Gérard , Vincent Alain 
Published: April 2021

ABSTRACT
A dramatic reorganization of the cytoskeleton underlies the cellularisation of the syncytial Drosophila embryo. Formation of a regular network of acto-myosin filaments, providing a structural framework, and possibly a contractile force as well, appears essential for the synchronous invagination of the plasma membrane between adjacent nuclei. The serendipity alpha (sry α) gene is required for this complete reorganization of the microfilaments at the onset of membrane invagination. We compare here the structure and expression of sry α between D. pseudoobscura, D. subobscura and D. melanogaster. Interspersion of evolutionarily highly conserved and divergent regions is observed in the protein. One such highly conserved region shows sequence similarities to a motif found in proteins of the ezrin-radixinmoesin (ERM) family. Four 7-13 bp motifs are conserved in the 5 promoter region; two of these are also found, and at the same position relative to the TATA box, in nullo, another zygotic gene recently shown to be involved in cellularisation. The compared patterns of expression of D. melanogaster sry and nullo, and D. pseudoobscura sry reveal a complex regulation of the spatiotemporal accumulation of their transcripts. The D. pseudoobscura sry gene is able to rescue the cellularisation defects associated with a complete loss of sry α function in D. melanogaster embryos, even though species-specific aspects of its expression are maintained. Despite their functional homologies, the D. melanogaster and D. pseudoobscura sry RNAs have different subcellular localisations, suggesting that this specific localization has no conserved role in targeting the sry α protein to the apical membranes.
v-erbA and citral reduce the teratogenic effects of all-trans retinoic acid and retinol, respectively, in Xenopus embryogenesis
Authors: Schuh Timothy J. , Hall Bonnie L. , Kraft Joan Creech , Privalsky Martin L. , Kimelman David 
Published: April 2021

ABSTRACT
Treatment of late blastula/early gastrula stage Xenopus embryos with all-trans retinoic acid results in disruption of the primary body axis through effects on both mesoderm and neuroectoderm. This effect of retinoic acid, coupled with the known presence of retinoic acid in Xenopus embryos has led to the proposal that retinoic acid may be an endogenous morphogen providing posi-tional information in early development. To further elucidate the role of retinoic acid in early Xenopus devel-opment, we have attempted to interfere with the retinoic acid signalling pathway both at the level of retinoic acid formation, by treatment with citral (3,7-dimethy-2,6-octadienal), and at the level of nuclear retinoic acid receptor function, by microinjection of v-erbA mRNA. The feasibility of this approach was demonstrated by the ability of citral treatment and v-erbA mRNA injection to reduce the teratogenic effects of exogenous retinol and retinoic acid, respectively, in early Xenopus develop-ment. Interestingly, v-erbA mRNA injection and citral treatment of gastrula stage embryos resulted in tadpoles with a similar set of developmental defects. The defects were chiefly found in tissues that received a contribution of cells from the neural crest, suggesting that at least a subset of neural crest cells may be sensitive to the endogenous level of retinoic acid. In accord with this proposal, it was found that the expression patterns of two early markers of cranial neural crest cells, Xtwi and XAP-2, were altered in embryos injected with v-erbA mRNA. These results indicate that structures in addition to the primary axis are regulated by retinoic acid sig-nalling during early Xenopus development.
Cell-cell interactions regulate skeleton formation in the sea urchin embryo
Authors: Armstrong Norris , Hardin Jeff , McClay David R. 
Published: April 2021

ABSTRACT
In the sea urchin embryo, the primary mesenchyme cells (PMCs) make extensive contact with the ectoderm of the blastula wall. This contact is shown to influence production of the larval skeleton by the PMCs. A previous observation showed that treatment of embryos with NiCl2 can alter spicule number and skeletal pattern (Hardin et al. (1992)Development, 116, 671-685). Here, to explore the tissue sensitivity to NiCl2, experiments recombined normal or NiCl2-treated PMCs with either normal or NiCl2-treated PMC-less host embryos. We find that NiCl2 alters skeleton production by influencing the ectoderm of the blastula wall with which the PMCs interact. The ectoderm is responsible for specifying the number of spicules made by the PMCs. In addition, experiments examining skeleton production in vitro and in half-and quarter-sized embryos shows that cell inter-actions also influence skeleton size. PMCs grown in vitro away from interactions with the rest of the embryo, can produce larger spicules than in vivo. Thus, the epithelium of the blastula wall appears to provide spatial and scalar information that regulates skeleton production by the PMCs.
The mouse homeodomain protein Phox2 regulates Ncam promoter activity in concert with Cux/CDP and is a putative determinant of neurotransmitter phenotype
Authors: Valarché Isabelle , Tissier-Seta Jean-Philippe , Hirsch Marie-Rose , Martinez Salvador , Goridis Christo , Brunet Jean-François 
Published: April 2021

ABSTRACT
Transcriptional regulation of the gene encoding the cell adhesion receptor NCAM (neural cell adhesion molecule), a putative effector molecule of a variety of morphogenetic events, is likely to involve important regulators of morphogenesis. Here we identify two mouse homeodomain proteins that bind to an upstream regulatory element in the Ncam promoter: Cux, related to Drosophila cut and human CDP, and Phox2, a novel protein with a homeodomain related to that of the Drosophila paired gene. In transient transfection experiments, Cux was found to be a strong inhibitor of Ncam promoter activity, and this inhibition could be relieved by simultaneously overexpressing Phox2. These results suggest that the Ncam gene might be a direct target of homeodomain proteins and provide a striking example of regulatory cross-talk between homeodomain proteins of different classes. Whereas the expression pattern of Cux/CDP includes many NCAM-negative sites, Phox2 expression was restricted to cells also expressing Ncam or their progenitors. The localisation data thus strongly reinforce the notion that Phox2 plays a role in transcriptional activation of Ncam in Phox2-positive cell types.
In the peripheral nervous system, Phox2 was strongly expressed in all ganglia of the autonomic nervous system and more weakly in some cranial sensory ganglia, but not in the sensory ganglia of the trunk. Phox2 transcripts were detected in the primordia of sympathetic ganglia as soon as they form. Phox2 expression in the brain was confined to spatially restricted domains in the hindbrain, which correspond to the noradrenergic and adrenergic nuclei once they are identifiable. All Phox2-expressing components of the peripheral nervous system are at least transiently adrenergic or noradrenergic. In the developing brain, Phox2 was expressed at all known locations of (nor)adrenergic neurones and of their precursors. These results suggest that Phox2, in addition to regulating the NCAM gene, may be part of the regulatory cascade that controls the differentiation of neurons towards this neurotransmitter phenotype.
Expression of tie-2, a member of a novel family of receptor tyrosine kinases, in the endothelial cell lineage
Authors: Schnürch Harald , Risau Werner 
Published: April 2021

ABSTRACT
We are interested in the molecular mechanisms that are involved in the development of the vascular system. In order to respond to morphogenetic and mitogenic signals, endothelial cells must express appropriate receptors. To characterize endothelial cell-specific receptors, we have concentrated on receptor tyrosine kinases, because several lines of evidence suggested the importance of controlled phosphotyrosine levels in endothelial cells. A strategy based on PCR amplification using degenerate oligonucleotides and mouse brain capillaries as mRNA source, led to the identification of a novel receptor tyrosine kinase, which we designated tie-2. In situ hybridization using a tie-2-specific probe revealed an interesting spatial and temporal expression pattern. The gene was expressed specifically in the endothelial lineage. tie-2 transcripts were present in endothelial cell precursors (angioblasts) and also in endothelial cells of sprouting blood vessels throughout development and in all organs and tissues so far examined. tie-2 was down-regulated in the adult. Because of the unusual combination of immunoglobulin, EGF-like and fibronectin type III domains in the extracellular portion of tie-2 which is shared by TEK and tie, these molecules may be considered members of a new family of receptor tyrosine kinases. Signal transduction via this new class of tyrosine kinases could lead to a better understanding of the molecular mechanisms of blood vessel formation.
IMP-L2: an essential secreted immunoglobulin family member implicated in neural and ectodermal development in Drosophila
Authors: Garbe James C. , Yang Eric , Fristrom James W. 
Published: April 2021

ABSTRACT
The Drosophila IMP-L2 gene was identified as a 20hydroxyecdysone-induced gene encoding a membranebound polysomal transcript. IMP-L2 is an apparent secreted member of the immunoglobulin superfamily. We have used deficiencies that remove the IMP-L2 gene to demonstrate that IMP-L2 is essential in Drosophila. The viability of IMP-L2 null zygotes is influenced by maternal IMP-L2. IMP-L2 null progeny from IMP-L2+ mothers exhibit a semilethal phenotype. IMP-L2 null progeny from IMP-L2 null mothers are 100% lethal. An IMP-L2 transgene completely suppresses the zygotic lethal phenotype and partially suppresses the lethality of IMP-L2 null progeny from IMP-L2 null mothers. In embryos, IMP-L2 mRNA is first expressed at the cellular blastoderm stage and continues to be expressed through subsequent development. IMP-L2 mRNA is detected in several sites including the ventral neuroectoderm, the tracheal pits, the pharynx and esophagus, and specific neuronal cell bodies. Staining of whole-mount embryos with anti-IMP-L2 antibodies shows that IMP-L2 protein is localized to specific neuronal structures late in embryogenesis. Expression of IMP-L2 protein in neuronal cells suggests a role in the normal development of the nervous system but no severe morphological abnormalities have been detected in IMP-L2 null embryos.
Programmed cell death in the Drosophila CNS is ecdysone-regulated and coupled with a specific ecdysone receptor isoform
Authors: Robinow Steven , Talbot William S. , Hogness David S. , Truman James W. 
Published: April 2021

ABSTRACT
At adult emergence, the ventral CNS of Drosophila shows a group of approximately 300 neurons, which are unique in that they express 10-fold higher levels of the A isoform of the ecdysone receptor (EcR-A) than do other central neurons. This expression pattern is established early in metamorphosis and persists throughout the remainder of the pupal stage. Although these cells represent a heterogeneous group of neurons, they all share the same fate of undergoing rapid degeneration after the adult emerges from the pupal case. One prerequisite for this death is the decline of ecdysteroids at the end of metamorphosis. Treatment of flies with 20hydroxyecdysone blocks the death of the cells, but only if given at least 3 hours before the normal time of degeneration. The correlation of a unique pattern of receptor isoform expression with a particular steroid-regulated fate suggests that variations in the pattern of receptor isoform expression may serve as important switches during development.
A dual role for the protein kinase shaggy in the repression of achaete- scute
Authors: Simpson Pat , Ruel Laurent , Heitzler Pascal , Bourouis Marc 
Published: April 2021

ABSTRACT
achaete and scute are expressed in a spatially restricted pattern and provide neural potential to cells, rhe domains of expression depend partly on extra- macrochaetae whose product is itself spatially restricted and acts as a negative post-translational regulator of achaete and scute. The protein kinase shaggy also represses achaete and scute at many sites hut may act via intermediate transcription factors. However shaggy and extramacrochaetae act synergistically and molecular studies suggest that they may be part of the same pathway, shaggy is functionally homologous to the mammalian glycogen synthase kinase-3 and analogy with the known physiology of this enzyme, suggests that this function of shaggy may result from the “constitu- tive” activity. At the site where a single neural precursor will develop, achaete and scute are initially expressed in a group of equivalent cells. ‘Hie genes Notch and Delta are part of a lateral signal required to single out one precursor cell and to silence achaete and scute expression in the other cells, shaggy is required downstream of Notch for transduction of the inhibitory signal., This second role of shaggy may be due to modulation of enzymatic activity during signalling.
A fate map of the epiblast of the early chick embryo
Authors: Hatada Yohko , Stern Claudio D. 
Published: April 2021

ABSTRACT
We have used carbocyanine dyes (DiI and DiO) to generate fate maps for the epiblast layer of the chick embryo between stage X and the early primitive streak stage (stages 2 –3).
The overall distribution of presumptive cell types in these maps is similar to that described for other laboratory species (zebrafish, frog, mouse). Our maps also reveal certain patterns of movement for these presumptive areas. Most areas converge towards the midline and then move anteriorly along it. Interestingly, however, some presumptive tissue types do not take part in these predominant movements, but behave in a different way, even if enclosed within an area that does undergo medial convergence and anterior movement. The apparently independent behaviour of certain cell populations suggests that at least some presumptive cell types within the epiblast are already specified at preprimitive streak stages.