bluuebunny/crossref_metadata_2025_split huggingface dataset:
Origins of the avian neural crest: the role of neural plate-epidermal interactions
Authors: Selleck Mark A. J. , Bronner-Fraser Marianne 
Published: April 2021

ABSTRACT
We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of nonneural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4-5) or later (stages 6-10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.
Apoptosis of the midline glia during Drosophila embryogenesis: a correlation with axon contact
Authors: Sonnenfeld Margaret J. , Jacobs J. Roger 
Published: April 2021

ABSTRACT
We have examined cell death within lineages in the midline of Drosophila embryos. Approximately 50% of cells within the anterior, middle and posterior midline glial (MGA, MGM and MGP) lineages died by apoptosis after separation of the commissural axon tracts. Glial apoptosis is blocked in embryos deficient for reaper, where greater than wild-type numbers of midline glia (MG) are present after stage 12. Quantitative studies revealed that MG death followed a consistent temporal pattern during embryogenesis. Apoptotic MG were expelled from the central nervous system and were subsequently engulfed by phagocytic haemocytes. MGA and MGM survival was apparently dependent upon proper axonal contact. In embryos mutant for the commissureless gene, a decrease in axon-glia contact correlated with a decrease in MGA and MGM survival and accelerated the time course of MG death. In embryos mutant for the slit gene, MGA and MGM maintained contact with longitudinally and contralaterally projecting axons and MG survival was comparable to that in wildtype embryos. The initial number of MG within individual ventral nerve cord segments was increased by ectopic expression of the rhomboid gene, without changing axon number. Extra MGA and MGM were eliminated from the ventral nerve cord by apoptosis to restore wild-type numbers of midline glia. Ectopic rhomboid expression also shifted MGA and MGM cell death to an earlier stage of embryogenesis. One possible explanation is that axon-glia contact or communication promotes survival of the MG and that MG death may result from a competition for available axon contact.
Initiation of the proximodistal axis in insect legs
Authors: Campbell Gerard , Tomlinson Andrew 
Published: April 2021

ABSTRACT
Much of the cell-cell communication that controls assignment of cell fates during animal development appears to be mediated by extracellular signaling molecules. The formation of the proximodistal (P/D) axis of the legs of flies is controlled by at least two such molecules, a Wnt and a TGFβ, encoded by the wingless (wg) and decapentaplegic (dpp) genes, respectively. The P/D axis appears to be initiated from the site where cells expressing wg are in close association with those expressing dpp. Support for this hypothesis comes from two sources: classical grafting experiments in cockroaches and ectopic protein expression in Drosophila.
Combinatorial signals from the neural tube, floor plate and notochord induce myogenic bHLH gene expression in the somite
Authors: Münsterberg Andrea E. , Lassar Andrew B. 
Published: April 2021

ABSTRACT
The neural tube, floor plate and notochord are axial tissues in the vertebrate embryo which have been demonstrated to play a role in somite morphogenesis. Using in vitro co-culture of tissue explants, we have monitored inductive interactions of these axial tissues with the adjacent somitic mesoderm in chick embryos. We have found that signals from the neural tube and floor plate/notochord are necessary for expression of the myogenic bHLH regulators MyoD, Myf5 and myogenin in the somite. Eventually somitic expression of the myogenic bHLH genes is main-tained in the absence of the axial tissues. In organ culture, at early developmental stages (HH 11-), induction of myogenesis in the three most recently formed somites can be mediated by the neural tube together with the floor plate/notochord, while in more rostral somites (stages IV-IX) the neural tube without the floor plate/notochord is sufficient. By recombining somites and neural tubes from different axial levels of the embryo, we have found that a second signal is necessary to promote competence of the somite to respond to inducing signals from the neural tube. Thus, we propose that at least two signals from axial tissues work in combination to induce myogenic bHLH gene expression; one signal derives from the floor plate/notochord and the other signal derives from regions of the neural tube other than the floor plate.
Homeobox genes and connective tissue patterning
Authors: Oliver Guillermo , Wehr Roland , Jenkins Nancy A. , Copeland Neal G. , Cheyette Benjamin N. R , Hartenstein Volker , Zipursky S. Lawrence , Gruss Peter 
Published: April 2021

ABSTRACT
In vertebrates, limb tendons are derived from cells that migrate from the lateral plate mesoderm during early development. While some of the developmental steps leading to the formation of these tissues are known, little is known about the molecular mechanisms controlling them. We have identified two murine homeobox-containing genes, Six 1 and Six 2, which are expressed in a complementary fashion during the development of limb tendons. Transcripts for both genes are found in different sets of phalangeal tendons. Six 1 and Six 2 also are expressed in skeletal and smooth muscle, respectively. These genes may participate in the patterning of the distal tendons of the limb phalanges by setting positional values along the limb axes.
Regulation of desmocollin transcription in mouse preimplantation embryos
Authors: Collins Jane E. , Lorimer Jo E. , Garrod David R. , Pidsley Sara C. , Buxton Roger S. , Fleming Tom P. 
Published: April 2021

ABSTRACT
The molecular mechanisms regulating the biogenesis of the first desmosomes to form during mouse embryogenesis have been studied. A sensitive modification of a reverse transcriptase - cDNA amplification procedure has been used to detect transcripts of the desmosomal adhesive cadherin, desmocollin. Sequencing of cDNA amplification products confirmed that two splice variants, a and b, of the DSC2 gene are transcribed coordinately. Transcripts were identified in unfertilized eggs and cumulus cells and in cleavage stages up to the early 8-cell stage, were never detected in compact 8-cell embryos, but were evident again either from the 16-cell morula or very early blastocyst (approx 32-cells) stages onwards. These two phases of transcript detection indicate DSC2 is encoded by maternal and embryonic genomes. Previously, we have shown that desmocollin protein synthesis is undetectable in eggs and cleavage stages but initiates at the early blastocyst stage when desmocollin localises at, and appears to regulate assembly of, nascent desmosomes that form in the trophectoderm but not in the inner cell mass (Fleming, T. P., Garrod, D. R. and Elsmore, A. J. (1991), Development 112, 527-539). Maternal DSC2 mRNA is therefore not translated and presumably is inherited by blastomeres before complete degradation. Our results suggest, however, that initiation of embryonic DSC2 transcription regulates desmocollin protein expression and thereby desmosome formation. Moreover, data from blastocyst single cell analyses suggest that embryonic DSC2 transcription is specific to the trophectoderm lineage. Inhibition of E-cadherin-mediated cell-cell adhesion did not influence the timing of DSC2 embryonic transcription and protein expression. However, isolation and culture of inner cell masses induced an increase in the amount of DSC2 mRNA and protein detected. Taken together, these results suggest that the presence of a contact-free cell surface activates DSC2 transcription in the mouse early embryo.
Analysis of the genetic hierarchy guiding wing vein development in Drosophila
Authors: Sturtevant Mark A. , Bier Ethan 
Published: April 2021

ABSTRACT
The Drosophila rhomboid (rho) and Egf- and r genes are members of a small group of genes required for the differ- and entiation of various specific embryonic and adult structures. During larval and early pupal development expression of rho in longitudinal vein primordia mediates the localized formation of wing veins. In this paper we investigate the genetic hierarchy guiding vein development, by testing for genetic interactions between rho alleles and a wide variety of wing vein mutations and by examining the pattern of rho expression in mutant developing wing primordia. We identify a small group of wing vein mutants that interact strongly with rho. Examination of rho expression in these and other key vein mutants reveals when vein development first becomes abnormal. Based on these data and on previous genetic analyses of vein formation we present a sequential model for establishment and differentiation of wing veins.
Identifying tumor suppressors in genetic mosaics: the Drosophila lats gene encodes a putative protein kinase
Authors: Xu Tian , Wang Weiyi , Zhang Sheng , Stewart Rodney A. , Yu Wan 
Published: April 2021

ABSTRACT
We have identified recessive overproliferation mutations by screening and examining clones of mutant cells in genetic mosaics of the fruitfly Drosophila melanogaster. This type of screen provides a powerful approach for identifying and studying potential tumor suppressors. One of the identified genes, lats, has been cloned and encodes a putative protein kinase that shares high levels of sequence similarity with three proteins in budding yeast and Neu-rospora that are involved in regulation of the cell cycle and growth. Mutations in lats cause dramatic overproliferation phenotypes and various developmental defects in both mosaic animals and homozygous mutants.
Scleraxis: a basic helix-loop-helix protein that prefigures skeletal formation during mouse embryogenesis
Authors: Cserjesi Peter , Brown Doris , Ligon Keith L. , Lyons Gary E. , Copeland Neal G. , Gilbert Debra J. , Jenkins Nancy A. , Olson Eric N. 
Published: April 2021

ABSTRACT
Members of the basic helix-loop-helix (bHLH) family of transcription factors have been shown to regulate growth and differentiation of numerous cell types. Cell-typespecific bHLH proteins typically form heterodimers with ubiquitous bHLH proteins, such as E12, and bind a DNA consensus sequence known as an E-box. We used the yeast two-hybrid system to screen mouse embryo cDNA libraries for cDNAs encoding novel cell-type-specific bHLH proteins that dimerize with E12. One of the cDNAs isolated encoded a novel bHLH protein, called scleraxis. During mouse embryogenesis, scleraxis transcripts were first detected between day 9.5 and 10.5 post coitum (p.c.) in the sclerotome of the somites and in mesenchymal cells in the body wall and limb buds. Subsequently, scleraxis was expressed at high levels within mesenchymal precursors of the axial and appendicular skeleton and in cranial mesenchyme in advance of chondrogenesis; its expression pattern in these cell types foreshadowed the developing skeleton. Prior to formation of the embryonic cartilaginous skeleton, scleraxis expression declined to low levels. As development proceeded, high levels of scleraxis expression became restricted to regions where cartilage and connective tissue formation take place. Scleraxis bound the E-box consensus sequence as a heterodimer with E12 and activated transcription of a reporter gene linked to its DNA-binding site. The expression pattern, DNA-binding properties and transcriptional activity of scleraxis suggest that it is a regulator of gene expression within mesenchymal cell lineages that give rise to cartilage and connective tissue.
Control of proliferation activation in quiescent neuroblasts of the Drosophila central nervous system
Authors: Datta Sumana 
Published: April 2021

ABSTRACT
Stem cell proliferation is controlled through cell cycle arrest and activation. In the central nervous system of Drosophila melanogaster, neuroblast quiescence and activation takes place in defined spatial and temporal patterns. Two genes have been identified that regulate the pattern of neuroblast quiescence and proliferation. ana, which has been previously described by Ebens and coworkers (Ebens, A., Garren, H., Cheyette, B. N. R. and Zipursky, S. L. (1993). Cell 74, 15–28), encodes a secreted glial glycoprotein that inhibits premature neuroblast proliferation. We previously showed that trolsd causes a dramatic drop in the number of dividing cells in the larval brain late in development. This study presents evidence that this decrease results from a failure to activate proliferation in the quiescent neuroblast population at the appropriate time. However, trolsd does not affect the maintenance of cell division in already dividing mushroom body neuroblasts. The quiescent optic lobe and thoracic neuroblasts affected by trolsd proliferate in a trol mutant background if they have been activated by a lack of the ana proliferation repressor, demonstrating that trolsd does not affect cellular viability, nor does trol represent a celltype-specific mitotic factor. This also shows that trol acts downstream of ana to activate proliferation of quiescent neuroblasts in an anadependent pathway, possibly by inactivating or bypassing the ana repressor. These results suggest that trol and ana are components of a novel developmental pathway for the control of cell cycle activation in quiescent neuroblasts.
The lurcher gene induces apoptotic death in cerebellar Purkinje cells
Authors: Norman Deborah J. , Feng Lei , Cheng Susie S. , Gubbay John , Chan Emily , Heintz Nathaniel 
Published: April 2021

ABSTRACT
In the neurologically mutant mouse strain lurcher (Lc), heterozygous animals display cell autonomous degeneration of cerebellar Purkinje cells beginning in the second postnatal week. During the course of our studies to identify the genetic lesion responsible for this disease (Norman et al., 1991), we have formulated an hypothesis suggesting that in Lc Purkinje cells homeostasis is sufficiently perturbed to lead to the activation of programmed cell death, thus resulting in neuronal loss and the consequent neurologic disease (Heintz, 1993). To address this possibility, we have examined the properties of Lc Purkinje cells as they die during the second postnatal week. Our light and electron microscopic studies demonstrate that dying Lc Purkinje cells exhibit the characteristic morphologic features of apoptosis, including nuclear condensation, axon beading and membrane blebbing. Using an in situ endlabeling method, we have also detected nicked nuclear DNA in these cells. Furthermore, we have examined the expression of the sulfated glycoprotein 2 (SGP2), whose mRNA is induced in both T-cells and prostate epithelial cells undergoing apoptotic death. We show by in situ hybridization that SGP2 is not expressed at detectable levels in normal Purkinje cells, but that its mRNA is present in Lc Purkinje cells prior to their death. Also expression of the Kv3.3b potassium channel, which marks the terminal phase of Purkinje cell differentiation, is evident in Lc Purkinje cells prior to their death. These data demonstrate that the Lc mutation induces apoptosis in cerebellar Purkinje cells following their maturation in postnatal cerebellum. Isolation of the Lc mutation and further analysis of its action in eliciting apoptosis can provide an important opportunity for understanding the etiology of neurodegenerative disease.
Developmental expression of the maternal protein XDCoH, the dimerization cofactor of the homeoprotein LFB1 (HNF1)
Authors: Pogge v. Strandmann Elke , Ryffel Gerhart U. 
Published: April 2021

ABSTRACT
The tissue-specific transcription factors LFB1 (HNF1) and LFB3 (vHNF1) mainly expressed in liver, kidney and intestine are homeoproteins that interact with the regulatory element HP1. The HP1 sequence constitutes one of the most important cis-acting elements in liver-specifically expressed genes, while its function in other cell types containing LFB1 and LFB3 is not fully understood. In mammals, LFB1 activity is modulated by DCoH, a cofactor that stimulates the LFB1 transactivation significantly. Using the rat cDNA probe, we cloned the corresponding Xenopus sequence XDCoH, encoding a 104 amino acid protein, that is 85% identical to the rat protein. XDCoH enhances the LFB1-dependent transactivation potential in transfection experiments and interacts in vitro directly with LFB1 and its variant form LFB3. The protein is detectable in liver and kidney extracts of adult frogs and in small amounts also in lung and stomach, organs expressing LFB1 and/or LFB3 protein as well.
To investigate the possible involvement of XDCoH in Xenopus development, we analyzed its temporal and spatial expression pattern during early embryogenesis. XDCoH is a maternal factor, although LFB1 is absent in the egg. In early cleavage stages, the protein is detectable in the cytoplasm of each blastomere and enters the nuclei of the cells as early as the zygotic transcription in the Xenopus embryo starts. The amount of XDCoH increases dramatically following neurulation, when the formation of liver, pronephros and other organs takes place. Whole-mount immunostaining demonstrates that, in the developing larvae, XDCoH is localized in the nuclei of the hepatocytes, the gut cells and the pronephric cells, tissues of mesodermal and endodermal origin known to contain LFB1 and LFB3. Surprisingly it is also present in the pigmented epithelium surrounding the eye of the embryo, which is derived from the anterior part of the ectodermal neural plates and lacks LFB1. The tissue distribution of XDCoH during embryogenesis suggests that XDCoH is involved in determination and differentiation of various unrelated cell types. It seems likely that XDCoH interaction is not only essential for the function of LFB1 and LFB3 but also for certain other transcription factors.
Anterior neurectoderm is progressively induced during gastrulation: the role of the Xenopus homeobox gene orthodenticle
Authors: Blitz Ira L. , Cho W. Y. 
Published: April 2021

ABSTRACT
In order to study the regional specification of neural tissue we isolated Xotx2, a Xenopus homolog of the Drosophila orthodenticle gene. Xotx2 is initially expressed in Spemann’s organizer and its expression is absent in the ectoderm of early gastrulae. As gastrulation proceeds, Xotx2 expression is induced in the overlying ectoderm and this domain of expression moves anteriorly in register with underlying anterior mesoderm throughout the remainder of gastrulation. The expression pattern of Xotx2 suggests that a wave of Xotx2 expression (marking anterior neurectoderm) travels through the ectoderm of the gastrula with the movement of underlying anterior (prechordal plate) mesoderm. This expression of Xotx2 is reminiscent of the Eyal-Giladi model for neural induction. According to this model, anterior neural-inducing signals emanating from underlying anterior mesoderm transiently induce anterior neural tissues after vertical contact with the overlying ectoderm. Further patterning is achieved when the ectoderm receives caudalizing signals as it comes in contact with more posterior mesoderm during subsequent gastrulation movements. Functional characterization of the Xotx2 protein has revealed its involvement in differentiation of the anterior-most tissue, the cement gland. Ectopic expression of Xotx2 in embryos induces extra cement glands in the skin as well as inducing a cement gland marker (XAG1) in isolated animal cap ectoderm. Microinjection of RNA encoding the organizer-specific homeodomain protein goosecoid into the ventral marginal zone results in induction of the Xotx2 gene. This result, taken in combination with the indistinguishable expression patterns of Xotx2 and goosecoid in the anterior mesoderm suggests that Xotx2 is a target of goosecoid regulation.
wingless induces transdetermination in developing Drosophila imaginal discs
Authors: Maves Lisa , Schubiger Gerold 
Published: April 2021

ABSTRACT
Drosophila imaginal discs, the precursors of the adult fly appendages, have been the subject of intensive developmental studies, particularly on cell determination. Cultured disc fragments are recognized not only for the ability to maintain their determined state through extra cell divisions but also for the ability to transdetermine, or switch to the determined state of a different disc. An understanding of transdetermination at a molecular level will provide further insight into the requirements for maintaining cell determination. We find that ectopic expression of the Drosophila gene wingless induces transdetermination of foreleg imaginal disc cells to wing cells. This transdetermination occurs in foreleg discs of developing larvae without disc fragmentation. The in situ-transdetermining cells localize to the dorsal region of the foreleg disc. This wingless-induced transdetermination event is remarkably similar to the leg-to-wing switch that occurs after leg disc culture. Thus we have identified a new approach to a molecular dissection of transdetermination.
Head formation in Hydra is different at apical and basal levels
Authors: Technau Ulrich , Holstein Thomas W. 
Published: April 2021

ABSTRACT
Hydra’s head is a compound structure with a hypostome at the apical extreme and a circle of tentacles more basally. During head regeneration, it is thought (P. M. Bode, T. A. Awad, O. Koizumi, Y. Nakashima, C. J. P. Grimmelikhuijzen and H. R. Bode (1988) Development 102, 223-235; R. Weinziger, L. M. Salgado, C. N. David and T. C. G. Bosch (1994) Development 120, 2511-2517) that the conditions for tentacle formation are fulfilled before those for hypostome formation. Using a new hypostome-specific marker, we have found that the order of hypostome and tentacle formation is variable. In regenerating basal tissue, the hypostome marker is expressed before tentacles appear but in apical tissue, the tentacles appear first. This observation appears inconsistent with current views but can be explained by a hierarchical model (H. Meinhardt (1993)Developmental Biology 157, 321-333) in which tentacles require an inductive influence of the hypostome. In basal regenerates, the hypostome forms first and then induces tentacles. In apical regenerates, inductive factor remains from the amputated hypostome, and tentacle may form before the new hypostome. We have also observed that the mode of expression of the tentacle marker differs in basal and apical tissue. In basal tissue, the marker first appears in the definitive tentacle zone; in apical tissue, the marker first appears in the position of the presumptive hypostome and is then displaced to its final position, as described by previous workers. This observation is also expected according to the above-cited model.