bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sonic hedgehog contributes to oligodendrocyte specification in the mammalian forebrain
Authors: Nery Susana , Wichterle Hynek , Fishell Gord 
Published: April 2021

Abstract
This study addresses the role of Sonic hedgehog (Shh) in promoting the generation of oligodendrocytes in the mouse telencephalon. We show that in the forebrain, expression of the early oligodendrocyte markers Olig2, plp/dm20 and PDGFRα corresponds to regions of Shh expression? To directly test if Shh can induce the development of oligodendrocytes within the telencephalon, we use retroviral vectors to ectopically express Shh within the mouse embryonic telencephalon. We find that infections with Shh-expressing retrovirus at embryonic day 9.5, result in ectopic Olig2 and PDGFRα expression by mid-embryogenesis. By postnatal day 21, cells expressing ectopic Shh overwhelmingly adopt an oligodendrocyte identity? To determine if the loss of telencephalic Shh correspondingly results in the loss of oligodendrocyte production, we studied Nkx2.1 mutant mice in which telencephalic expression of Shh is selectively lost. In accordance with Shh playing a role in oligodendrogenesis, within the medial ganglionic eminence ofNkx2.1 mutants, the early expression of PDGFRα is absent and the level of Olig2 expression is diminished in this region. In addition, in these same mutants, expression of both Shh and plp/dm20 is lost in the hypothalamus. Notably, in the prospective amygdala region where Shh expression persists in the Nkx2.1 mutant, the presence of plp/dm20 is unperturbed. Further supporting the idea that Shh is required for the in vivo establishment of early oligodendrocyte populations, expression of PDGFRα can be partially rescued by virally mediated expression of Shh in the Nkx2.1 mutant telencephalon. Interestingly, despite the apparent requirement for Shh for oligodendrocyte specification in vivo, all regions of either wild-type or Nkx2.1 mutant telencephalon are competent to produce oligodendrocytes in vitro. Furthermore, analysis of CNS tissue from Shh null animals definitively shows that, in vitro, Shh is not required for the generation of oligodendrocytes. We propose that oligodendrocyte specification is negatively regulated in vivo and thatShh generates oligodendrocytes by overcoming this inhibition. Furthermore, it appears that a Shh-independent pathway for generating oligodendrocytes exists.
The cell adhesion molecule Echinoid defines a new pathway that antagonizes the Drosophila EGF receptor signaling pathway
Authors: Bai Jia-Min , Chiu Wei-Hsin , Wang Jiunn-Chin , Tzeng Ting-Hue , Perrimon Norbert , Hsu Jui-Chou 
Published: April 2021

ABSTRACT
Photoreceptor and cone cells in the Drosophila eye are recruited following activation of the epidermal growth factor receptor (EGFR) pathway. We have identified echinoid (ed) as a novel putative cell adhesion molecule that negatively regulates EGFR signaling. The ed mutant phenotype is associated with extra photoreceptor and cone cells. Conversely, ectopic expression of ed in the eye leads to a reduction in the number of photoreceptor cells. ed expression is independent of EGFR signaling and ED is localized to the plasma membrane of every cells throughout the eye disc. We present evidence that ed acts nonautonomously to generate extra R7 cells by a mechanism that is sina-independent but upstream of Tramtrack (TTK88). Together, our results support a model whereby ED defines an independent pathway that antagonizes EGFR signaling by regulating the activity, but not the level, of the TTK88 transcriptional repressor.
Merlin, the Drosophila homologue of neurofibromatosis-2, is specifically required in posterior follicle cells for axis formation in the oocyte
Authors: MacDougall Nina , Lad Yatish , Wilkie Gavin S. , Francis-Lang Helen , Sullivan William , Davis Ilan 
Published: April 2021

ABSTRACT
In Drosophila, the formation of the embryonic axes is initiated by Gurken, a transforming growth factor α signal from the oocyte to the posterior follicle cells, and an unknown polarising signal back to the oocyte. We report that Drosophila Merlin is specifically required only within the posterior follicle cells to initiate axis formation. Merlin mutants show defects in nuclear migration and mRNA localisation in the oocyte. Merlin is not required to specify posterior follicle cell identity in response to the Gurken signal from the oocyte, but is required for the unknown polarising signal back to the oocyte. Merlin is also required non-autonomously, only in follicle cells that have received the Gurken signal, to maintain cell polarity and limit proliferation, but is not required in embryos and larvae. These results are consistent with the fact that human Merlin is encoded by the gene for the tumour suppressor neurofibromatosis-2 and is a member of the Ezrin-Radixin-Moesin family of proteins that link actin to transmembrane proteins. We propose that Merlin acts in response to the Gurken signal by apically targeting the signal that initiates axis specification in the oocyte.
A bipotential precursor population for pancreas and liver within the embryonic endoderm
Authors: Deutsch Gail , Jung Joonil , Zheng Minghua , Lóra José , Zaret Kenneth S. 
Published: April 2021

ABSTRACT
The pancreas emerges independently from dorsal and ventral domains of embryonic gut endoderm. Gene inactivation experiments in mice have identified factors required for dorsal pancreas development, but factors that initiate the ventral pancreas have remained elusive. In this study, we investigated the hypothesis that the emergence of the ventral pancreas is related to the emergence of the liver. We find that the liver and ventral pancreas are specified at the same time and in the same general domain of cells. Using embryo tissue explantation experiments, we find that the default fate of the ventral foregut endoderm is to activate the pancreas gene program. FGF signalling from the cardiac mesoderm diverts this endoderm to express genes for liver instead of those for pancreas. No evidence was found to indicate that the cell type choice for pancreas or liver involves a selection for growth or viability. Cardiac mesoderm or FGF induces the local expression of sonic hedgehog, which in turn is inhibitory to pancreas but not to liver. The bipotential precursor cell population for pancreas and liver in embryonic development and its fate selection by FGF has features that appear to be recapitulated in the adult pancreas and are reflected in the evolution of these organs.
Expression of activated Ras during Dictyostelium development alters cell localization and changes cell fate
Authors: Jaffer Zahara M. , Khosla Meenal , Spiegelman George B. , Weeks Gerald 
Published: April 2021

ABSTRACT
There is now a body of evidence to indicate that Ras proteins play important roles in development. Dictyostelium expresses several ras genes and each appears to perform a distinct function. Previous data had indicated that the overexpression of an activated form of the major developmentally regulated gene, rasD, caused a major aberration in morphogenesis and cell type determination. We now show that the developmental expression of an activated rasG gene under the control of the rasD promoter causes a similar defect. Our results indicate that the expression of activated rasG in prespore cells results in their transdifferentiation into prestalk cells, whereas activated rasG expression in prestalk causes gross mislocalization of the prestalk cell populations.
Rescuing desmoplakin function in extra-embryonic ectoderm reveals the importance of this protein in embryonic heart, neuroepithelium, skin and vasculature
Authors: Gallicano G. Ian , Bauer Christoph , Fuchs Elaine 
Published: April 2021

ABSTRACTDesmosomes mediate intercellular adhesion through desmosomal cadherins, which interface with plakoglobin (PG) and desmoplakin (DP) to associate with the intermediate filament (IF) cytoskeleton. Desmosomes first assemble in the E3.5 mouse trophectoderm, concomitant with establishment of epithelial polarity and appearance of a blastocoel cavity. Increasing in size and number, desmosomes continue their prominence in extra-embryonic tissues, but as development proceeds, they also become abundant in a number of embryonic tissues, including heart muscle, epidermis and neuroepithelium. Previously, we explored the functional importance of desmosomes by ablating the Dsp gene. Homozygous Dsp mutant embryos progressed through implantation, but did not survive beyond E6.5, owing to a loss or instability of desmosomes and tissue integrity. We have now rescued the extra-embryonic tissues by aggregation of tetraploid (wild-type) and diploid (Dsp mutant) morulae. These animals survive several days longer, but die shortly after gastrulation, with major defects in the heart muscle, neuroepithelium and skin epithelium, all of which possess desmosomes, as well as the microvasculature, which does not. Interestingly, although wild-type endothelial cells of capillaries do not form desmosomes, they possess unusual intercellular junctions composed of DP, PG and VE-cadherin. The severity in phenotype and the breadth of defects in the Dsp mutant embryo is greater than PG mutant embryos, substantiating redundancy between PG and other armadillo proteins (e.g. β-catenin). The timing of lethality is similar to that of the VE-cadherin null embryo, suggesting that a participating cause of death may be a defect in vasculature, not reported for PG null embryos.
Specification of left-right asymmetry in the embryonic gut of Drosophila
Authors: Ligoxygakis Petros , Strigini Maura , Averof Michalis 
Published: April 2021

ABSTRACT
Most animals exhibit stable left-right asymmetries in their body. Although significant progress has been made in elucidating the mechanisms that set up these asymmetries in vertebrates, nothing is known about them in Drosophila. This is usually attributed to the fact that no reversals of stable left-right asymmetries have been observed in Drosophila, although relevant surveys have been carried out. We have focused on the asymmetry of the proventriculus in the embryonic gut of Drosophila, an aspect of left-right asymmetry that is extremely stable in wild-type flies. We show that this asymmetry can be reversed by mutations in the dicephalic and wunen genes, which also cause reversals in the antero-posterior axis of the embryo relative to its mother. This is the first observation to suggest that left-right asymmetries in Drosophila can be reversed by genetic/developmental manipulations. It also suggests that maternal signals may initiate the specification of some left-right asymmetries in the embryo.
PAR-1 is required for the maintenance of oocyte fate in Drosophila
Authors: Huynh Jean-René , Shulman Joshua M. , Benton Richard , Johnston Daniel St 
Published: April 2021

ABSTRACT
The PAR-1 kinase is required for the posterior localisation of the germline determinants in C. elegans and Drosophila, and localises to the posterior of the zygote and the oocyte in each case. We show that Drosophila PAR-1 is also required much earlier in oogenesis for the selection of one cell in a germline cyst to become the oocyte. Although the initial steps in oocyte determination are delayed, three markers for oocyte identity, the synaptonemal complex, the centrosomes and Orb protein, still become restricted to one cell in mutant clones. However, the centrosomes and Orb protein fail to translocate from the anterior to the posterior cortex of the presumptive oocyte in region 3 of the germarium, and the cell exits meiosis and becomes a nurse cell. Furthermore, markers for the minus ends of the microtubules also fail to move from the anterior to the posterior of the oocyte in mutant clones. Thus, PAR-1 is required for the maintenance of oocyte identity, and plays a role in microtubule-dependent localisation within the oocyte at two stages of oogenesis. Finally, we show that PAR-1 localises on the fusome, and provides a link between the asymmetry of the fusome and the selection of the oocyte.
Distinct sites of origin of oligodendrocytes and somatic motoneurons in the chick spinal cord: oligodendrocytes arise from Nkx2.2-expressing progenitors by a Shh-dependent mechanism
Authors: Soula Cathy , Danesin Cathy , Kan Paulette , Grob Magali , Poncet Christian , Cochard Philippe 
Published: April 2021

ABSTRACT
In the vertebrate spinal cord, oligodendrocytes arise from the ventral part of the neuroepithelium, a region also known to generate somatic motoneurons. The emergence of oligodendrocytes, like that of motoneurons, depends on an inductive signal mediated by Sonic hedgehog. We have defined the precise timing of oligodendrocyte progenitor specification in the cervico-brachial spinal cord of the chick embryo. We show that ventral neuroepithelial explants, isolated at various development stages, are unable to generate oligodendrocytes in culture until E5 but become able to do so in an autonomous way from E5.5. This indicates that the induction of oligodendrocyte precursors is a late event that occurs between E5 and E5.5, precisely at the time when the ventral neuroepithelium stops producing somatic motoneurons. Analysis of the spatial restriction of oligodendrocyte progenitors, evidenced by their expression of O4 or PDGFRμ, indicate that they always lie within the most ventral Nkx2.2-expressing domain of the neuroepithelium, and not in the adjacent domain characterized by Pax6 expression from which somatic motoneurons emerge. We then confirm that Shh is necessary between E5 and E5.5 to specify oligodendrocyte precursors but is no longer required beyond this stage to maintain ongoing oligodendrocyte production. Furthermore, Shh is sufficient to induce oligodendrocyte formation from ventral neuroepithelial explants dissected at E5. Newly induced oligodendrocytes expressed Nkx2.2 but not Pax6, correlating with the in vivo observation. Altogether, our results show that, in the chick spinal cord, oligodendrocytes originate from Nkx2.2-expressing progenitors.
Notch signaling represses the glial fate in fly PNS
Authors: Van De Bor Véronique , Giangrande Angela 
Published: April 2021

ABSTRACT
By using gain-of-function mutations it has been proposed that vertebrate Notch promotes the glial fate. We show in vivo that glial cells are produced at the expense of neurons in the peripheral nervous system of flies lacking Notch and that constitutively activated Notch produces the opposite phenotype. Notch acts as a genetic switch between neuronal and glial fates by negatively regulating glial cell deficient/glial cells missing, the gene required in the glial precursor to induce gliogenesis. Moreover, Notch represses neurogenesis or gliogenesis, depending on the sensory organ type. Numb, which is asymmetrically localized in the multipotent cell that produces the glial precursor, induces glial cells at the expense of neurons. Thus, a cell- autonomous mechanism inhibits Notch signaling.
Steroid regulation of autophagic programmed cell death during development
Authors: Lee Cheng-Yu , Baehrecke Eric H. 
Published: April 2021

ABSTRACT
Apoptosis and autophagy are morphologically distinct forms of programmed cell death. While autophagy occurs during the development of diverse organisms and has been implicated in tumorigenesis, little is known about the molecular mechanisms that regulate this type of cell death. Here we show that steroid-activated programmed cell death of Drosophila salivary glands occurs by autophagy. Expression of p35 prevents DNA fragmentation and partially inhibits changes in the cytosol and plasma membranes of dying salivary glands, suggesting that caspases are involved in autophagy. The steroid-regulated BR-C, E74A and E93 genes are required for salivary gland cell death. BR-C and E74A mutant salivary glands exhibit vacuole and plasma membrane breakdown, but E93 mutant salivary glands fail to exhibit these changes, indicating that E93 regulates early autophagic events. Expression of E93 in embryos is sufficient to induce cell death with many characteristics of apoptosis, but requires the H99 genetic interval that contains the rpr, hid and grim proapoptotic genes to induce nuclear changes diagnostic of apoptosis. In contrast, E93 expression is sufficient to induce the removal of cells by phagocytes in the absence of the H99 genes. These studies indicate that apoptosis and autophagy utilize some common regulatory mechanisms.
TheC. eleganshomolog of the murine cystic kidney disease geneTg737functions in a ciliogenic pathway and is disrupted inosm-5mutant worms
Authors: Haycraft Courtney J. , Swoboda Peter , Taulman Patrick D. , Thomas James H. , Yoder Bradley K. 
Published: April 2021

ABSTRACTCilia and flagella are important organelles involved in diverse functions such as fluid and cell movement, sensory perception and embryonic patterning. They are devoid of protein synthesis, thus their formation and maintenance requires the movement of protein complexes from the cytoplasm into the cilium and flagellum axoneme by intraflagellar transport (IFT), a conserved process common to all ciliated or flagellated eukaryotic cells. We report that mutations in the Caenorhabditis elegans gene Y41g9a.1 are responsible for the ciliary defects in osm-5 mutant worms. This was confirmed by transgenic rescue of osm-5(p813) mutants using the wild-type Y41g9a.1 gene. osm-5 encodes a tetratricopeptide repeat (TPR)-containing protein that is the homolog of murine polaris (Tg737), a protein associated with cystic kidney disease and left-right axis patterning defects in the mouse. osm-5 is expressed in ciliated sensory neurons in C. elegans and its expression is regulated by DAF-19, an RFX-type transcription factor that governs the expression of other genes involved in cilia formation in the worm. Similar to murine polaris, the OSM-5 protein was found to concentrate at the cilium base and within the cilium axoneme as shown by an OSM-5::GFP translational fusion and immunofluorescence. Furthermore, time-lapse imaging of OSM-5::GFP fusion protein shows fluorescent particle migration within the cilia. Overall, the data support a crucial role for osm-5 in a conserved ciliogenic pathway, most likely as a component of the IFT process.Movies available on-line:http://www.biologists.com/Development/movies/dev3342.html
Hedgehog signaling patterns the tracheal branches
Authors: Glazer Lillian , Shilo Ben-Zion 
Published: April 2021

ABSTRACT
The elaborate branching pattern of the Drosophila tracheal system originates from ten tracheal placodes on both sides of the embryo, each consisting of about 80 cells. Simultaneous cell migration from each tracheal pit in six different directions gives rise to the stereotyped branching pattern. Each branch contains a fixed number of cells. Previous work has shown that in the dorsoventral axis, localized activation of the Dpp, Wnt and EGF receptor (DER) pathways, subdivides the tracheal pit into distinct domains. We present the role of the Hedgehog (Hh) signaling system in patterning the tracheal branches. Hh is expressed in segmental stripes abutting the anterior border of the tracheal placodes. Induction of patched expression, which results from activation by Hh, demonstrates that cells in the anterior half of the tracheal pit are activated. In hh-mutant embryos migration of all tracheal branches is absent or stalled. These defects arise from a direct effect of Hh on tracheal cells, rather than by indirect effects on patterning of the ectoderm. Tracheal cell migration could be rescued by expressing Hh only in the tracheal cells, without rescuing the ectodermal defects. Signaling by several pathways, including the Hh pathway, thus serves to subdivide the uniform population of tracheal cells into distinct cell types that will subsequently be recruited into the different branches.
Somite necrosis and developmental malformations induced by vitamin A in the golden hamster
Authors: Marin-Padilla Miguel , Ferm Vergil H. 
Published: April 2021

ABSTRACT
A simple method for the induction of developmental malformation in the golden hamster is presented. The teratogenic agent used consists of a single dose of vitamin A. Correlations between the day of gestation at which the vitamin A is administered and the type and percentage of malformations induced are reported. Young embryos obtained from treated mothers on the 8th day of gestation show somite necrosis within 12 hr. of the administration of vitamin A, reaching its maximum at 24 hr. The somite necrosis is considered to be a basic alteration resulting in an abnormal axial mesoderm which then fails to fulfil its function of lodging and protecting the neural tube. The unprotected and exposed neural tissue secondarily degenerates. Somite necrosis is considered to be the primary defect induced by vitamin A causing developmental malformations such as cranioschisis and sacral rachischisis. When somite necrosis occurs before neural tube closure extensive degeneration of the neural tube follows (e.g. cranioschisis). Somite necrosis occurring after closure of neural tube results in only minimal change in the neural tube (e.g. occult sacral rachischisis). Notochordal alterations (hypertrophy and necrosis) are also found in the young hamster embryo after administration of vitamin A to their mother on the 8th day of gestation.
The relationship between oöcyte and follicle in the hen’s ovary as shown by electron microscopy
Authors: Bellairs Ruth 
Published: April 2021

ABSTRACT
In the early stages of oogenesis, the follicle cells contain a ‘complex mass’ of organelles which from its size and position apparently corresponds with the region identified as Golgi body by authors using light microscopy. It contains paired centrioles, radiating tubules, patches of Golgi apparatus and an orderly series of stacks of rough-surfaced endoplasmic reticulum which contain a granular material. It is concluded that these cells are probably secretory. The ‘complex mass’ disappears in the final stages of oogenesis. Using the methyl-green-pyronin test, the follicle cells have been shown to be rich in ribonucleoproteins. Specialized structures termed ‘lining bodies’ are found at irregular intervals at the surfaces of the follicle cells where they abut on to each other or on to the oöcyte. Long processes from the follicle cells indent the surface of the oöcyte, bearing lining bodies with them. Although there is no direct evidence that these lining bodies become engulfed by the oöcyte, nevertheless structures that are found several microns deep within the oöcyte so closely resemble the lining bodies that it seems probable they are derived from them. The available evidence does not support the ideas of Schjeide and his coworkers that the lining bodies give rise to mitochondria. No evidence was found of intercellular bridges between follicle and oöcyte. At first, the follicle and oöcyte membranes lie close together. Gradually, villous-like elevations arise on the oöcyte cell membrane which increase in number and in height. These constitute the zona radiata. Vesicles, containing a granular material, are common in the cortical region of the oöcyte. It is possible that these are formed by pinocytosis, for pinocytoticlike invaginations of the oöcyte cell membrane are visible. These are especially apparent in the zona radiata. The inner layer of the vitelline membrane forms between the follicle and zona radiata, and at first appears to be moulded around projections of the follicle cells. Just before ovulation the cell membrane of the ovum appears to become fragmented into a series of large vacuoles at the cell surface.
Etude au microscope électronique de la réaction corticale: I. La reaction corticale de fécondation chez Paracentrotus et sa chronologie.: II. La réaction corticale de l’oeuf vierge de Sabellaria alveolata
Authors: Pasteels par Jean J. 
Published: April 2021

ABSTRACT

An electron microscope study of the cortical reaction

Paracentrotus lividus

Sabellaria alveolata

General conclusions