bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nuclear transfer from teratocarcinoma cells into mouse oocytes and eggs
Authors: Modlinski J. A. , Gerhäuser D. , Lioi B. , Winking H. , Illmensee K. 
Published: April 2021

Abstract
A spontaneous ovarian teratocarcinoma was isolated from a LT/Sv mouse female and converted into an ascites tumor from which embryonal carcinoma (EC) cells were dissociated. Non-enucleated and enucleated, activated oocytes were fused with EC cells and either cultured in vitro or transferred into ligated oviducts of Swiss/A females. The nucleocytoplasmic hybrids cultured in vitro up to 22 h were examined cytologically at various time intervals. EC nuclei showed morphological remodelling in the foreign cytoplasm. EC chromosomes and female pronuclear chromosomes together formed a common metaphase. The nucleocytoplasmic hybrids developed in vivo were analyzed cytologically between the first and third day after oviduct transfer. The majority of embryos developed abnormally and, in a few instances, they had passed several cleavage divisions and reached, at best, a developmental stage resembling a premature morula. Fertilized, enucleated eggs were fused with EC cells or microinjected with EC nuclei. The resulting nucleocytoplasmic hybrids were either cultured in vitro or in vivo up to the fourth day. Enzyme tests were carried out on the nuclear transplant embryos, using electrophoretic variants of glucose phosphate isomerase (GPI) in order to distinguish between EC nuclei (GPI-A) and recipient eggs (GPI-B). The EC-specific GPI could be detected in about one third of the embryos analyzed and, in several instances, also together with the egg-specific GPI. Most of them were arrested during early cleavage divisions. Some embryos cleaved abnormally or mimicked normal embryogenesis. In a few instances, development resulted in embryos that resembled late preimplantation embryos.
Mechanisms of pigment pattern formation in the quail embryo
Authors: Richardson Michael K. , Hornbruch Amata , Wolpert Lewis 
Published: April 2021

ABSTRACT
One hypothesis to account for pigment patterning in birds is that neural crest cells migrate into all feather papillae. Local cues then act upon the differentiation of crest cells into melanocytes. This hypothesis is derived from a study of the quail-chick chimaera (Richardson et al., Development 107, 805–818, 1989). Another idea, derived from work on larval fish and amphibia, is that pigment patterns arise from the differential migration of crest cells. We want to know which of these mechanisms can best account for pigment pattern formation in the embryonic plumage of the quail wing. Most of the feather papillae on the dorsal surface of the wing are pigmented, while many on the ventral surface are white.
When ectoderm from unpigmented feather papillae is grown in culture, it gives rise to melanocytes. This indicates that neural crest cells are present in white feathers but that they fail to differentiate. If the wing tip is inverted experimentally then the pigment pattern is inverted also. This is difficult to explain in terms of a model based on migratory pathways, unless one assumes that the pathways became re-routed.
When an extra polarizing region is grafted to the anterior margin of the wing bud, a duplication develops in: (1) the pattern of skeletal elements; (2) the pattern of feather papillae; (3) the feather pigment pattern. The pigment pattern was not a precise mirror image although some groups of papillae showed a high degree of symmetry in their pigmentation. Both the tip inversions and the duplications produce discontinuities in the feather and pigment patterns. No evidence of intercalation was found in these cases. We conclude that pigment patterning in birds is determined by local cues acting on melanocyte differentiation, rather than by the differential migration of crest cells. Positional values along the anteroposterior axis of the pigment pattern are determined by a gradient of positional information. Thus the pigment patterns, feather patterns and cartilage patterns of the wing may all be specified by a similar mechanism.
Three markers of adult non-myelin-forming Schwann cells, 217c(Ran-1), A5E3 and GFAP: development and regulation by neuron–Schwann cell interactions
Authors: Jessen K. R. , Morgan L. , Stewart H. J. S. , Mirsky R. 
Published: April 2021

ABSTRACT
Immunohistochemical methods are used to investigate in detail the development and regulation of three proteins (217c(Ran-1),A5E3 and GFAP) specifically associated with adult non-myelin-forming Schwann cells in the rat sciatic nerve, from embryo day 15 to maturity. 217c(Ran-1),which is probably the NGF-receptor, and A5E3 are expressed by the majority of cells in the nerve at embryo day 15 and by essentially all cells at embryo day 18. GFAP first appears at embryo day 18; this is an intrinsically programmed developmental event which occurs in cultured Schwann cells even in the absence of serum. Postnatally, the expression of 217c(Ran-1),A5E3 and GFAP is suppressed in cells that form myelin but retained in non-myelin-forming Schwann cells. Mature myelin-forming cells nevertheless maintain the potential to express all three proteins but will only do so if removed from contact with myelinated axons. In neuron-free cultures Schwann cells express all three proteins.
This work, together with our previous observations on N-CAM, shows that removal of a diverse set of surface proteins and a change in intermediate filament expression is one of the major consequences of axon to Schwann cell signalling during myelination in the rat sciatic nerve. Unlike myelin-forming cells, adult nonmyelin-forming Schwann cells remain very similar to embryonic and newborn cells with respect to expression of surface proteins, in contrast to the previously established developmental changes that occur in their surface lipids.
Fetal and adult localization of C/EBP: evidence for combinatorial action of transcription factors in cell-specific gene expression
Authors: Kuo C. Frank , Xanthopoulos Kleanthis G. , Darnell James E. 
Published: April 2021

ABSTRACT
C/EBP is a positive-acting transcription factor important for hepatocyte-specific expression present not only in hepatocytes but also a limited number of other cell types in adult mice. By Northern blot analysis and in situ hybridization experiments with mouse embryos and adult tissues, we first detected C/EBP mRNA in hepatocytes at the 13th gestational day, when no other cell types give detectable signals and thus by this test C/EBP is, at least in the embryo, a ‘liver-specific’ factor. Only trace amounts of C/EBP were seen in the yolk sac and no mRNA was detectable in choroid plexus in either embryos or adult animals. Both these cell types produce some proteins (e.g. albumin, transthyretin, a-l antitrypsin and others) that are also made in the liver where C/EBP is important for their production; thus either fewer factors or different factors govern yolk sac and choroid plexus production of these proteins. C/EBP mRNA was not detected in fetal brain but was present in several regions of the adult mouse brain again emphasizing that this factor does not appear to have a very early embryologic role. In the adult brain, it was most concentrated in CAI to CA4 regions of the hippocampus, in cerebellar Purkinje cells, and in layer II and III of the cortex.
Structural and compositional divergencies in the extracellular matrix encountered by neural crest cells in the white mutant axolotl embryo
Authors: Perris R. , Löfberg J. , FällströM C. , Boxberg Y. Von , Olsson L. , Newgreen D. F. 
Published: April 2021

ABSTRACT
The skin of the white mutant axolotl larva is pigmented differently from that of the normal dark due to a local inability of the extracellular matrix (ECM) to support subepidermal migration of neural crest-derived pigment cell precursors. In the present study, we have compared the ECM of neural crest migratory pathways of normal dark and white mutant embryos ultrastructurally, immunohistochemically and biochemically to disclose differences in their structure/composition that could be responsible for the restriction of subepidermal neural crest cell migration in the white mutant axolotl. When examined by electron microscopy, in conjunction with computerized image analysis, the structural assembly of interstitial and basement membrane ECMs of the two embryos was found to be largely comparable. At stages of initial neural crest cell migration, however, fixation of the subepidermal ECM in situ with either Karnovsky-ruthenium red or with periodate-lysine-paraform-aldehyde followed by ruthenium red-containing fixatives, revealed that fibrils of the dark matrix were significantly more abundant in associated electron-dense granules. This ultrastructural discrepancy of the white axolotl ECM was specific for the subepidermal region and suggested an abnormal proteoglycan distribution. Dark and white matrices of the medioventral migratory route of neural crest cells had a comparable appearance but differed from the corresponding subepidermal ECMs. Immunohistochemistry revealed only minor differences in the distribution of fibronectin, laminin, collagen types I, and IV, whereas collagen type III appeared differentially distributed in the two embryos. Chondroitin- and chondroitin-6-sulfate-rich proteogly cans were more prevalent in the white mutant embryo than in the dark, especially in the subepidermal space. Membrane microcarriers were utilized to explant site-specifically native ECM for biochemical analysis. Two dimensional gel electrophoresis of these regional matrices revealed a number of differences in their protein content, principally in constituents of apparent molecular masses of 30– 90 000. Taken together our observations suggest that local divergences in the concentration/assembly of low and high molecular mass proteins and proteoglycans of the ECM encountered by the moving neural crest cells account for their disparate migratory behavior in the white mutant axolotl.
Different patterns of transcription from the two Antennapedia promoters during Drosophila embryogenesis
Authors: Bermingham John R. , Martinez-Arias Alfonso , Petitt Matthew G. , Scott Matthew P. 
Published: April 2021

ABSTRACT
The homeotic genes of Drosophila control the differentiation of segments during development. Mutations in these genes cause one or more segments to develop structures normally found elsewhere in the organism. Several studies have shown that the spatial patterns of homeotic gene transcription are highly complex, and that these precise patterns of transcription are critical to normal development. The homeotic gene Antennapedia (Antp), a member of the Antennapedia Complex, is required for the correct differentiation of thoracic segments in both embryos and adults. The patterns of total Antp transcript and protein accumulation have been described in detail, but the contribution of each promoter to the overall pattern in embryos has not been reported. We have examined in detail the spatial distribution of transcripts from each of the Antp promoters in both embryo sections and whole embryos by in situ hybridization using promoter-specific probes. We show that the transcripts from each of the two promoters accumulate in distinct, but overlapping patterns during embryogenesis. The results demonstrate that the two Antp promoters are differentially regulated in embryos and provide a basis for examining the regulation of the two promoters and characterizing more fully the func tion of Antp during embryogenesis. In addition, we have examined the regulation of each of the Antp promoters by genes of the bithorax complex (BX-C). We show that in BX-C− embryos both promoters are derepressed in the abdomen.
Effects of the lethal yellow (AY) mutation in mouse aggregation chimeras
Authors: Barsh Gregory S. , Lovett Michael , Epstein Charles J. 
Published: April 2021

ABSTRACT
The Ay allele is a recessive lethal mutation at the mouse agouti locus, which results in embryonic death around the time of implantation. In the heterozygous state, Ay produces several dominant pleiotropic effects, including an increase in weight gain and body length, a susceptibi lity to hepatic, pulmonary and mammary tumors, and a suppression of the agouti phenotype, which results in a yellow coat color. To investigate the cellular action of Ay with regard to its effects upon embryonic viability and adult-onset obesity, we generated a series of aggregation chimeras using embryos that differ in their agouti locus genotype. Embryos derived from Ay/a×X.Ay/a matings were aggregated with those derived from A/A × A/A matings, and genotypic identification of the resultant chimeras was accomplished using a molecular probe at the Emv-15 locus that distinguishes among the three different alleles, Ay, A, and a. Among 50 chimeras, 25 analyzed as liveborns and 25 as 9.5 day embryos, 29 were a/a ↔ A/A and 21 were Ay/a ↔ A/A. The absence of AyIAy↔ A/A chimeras demonstrates that Ay/Ay cells cannot be rescued in a chimeric environment, and the relative deficiency of Ay/a ↔ A/A chimeras suggests that, under certain conditions, Ay heterozygosity may par tially affect cell viability or proliferation. In the 25 liveborn chimeras, Ay/a ↔ A/A animals became obese as adults and a/a ↔ A/A animals did not. There was no correlation between genotypic proportions and rate of weight gain, which shows that, with regard to its effects on weight gain, Ay heterozygosity is cell non-auton-omous.
Coexistence of perinatal and adult forms of a glial progenitor cell during development of the rat optic nerve
Authors: Wolswijk Guus , Riddle Peter N. , Noble Mark 
Published: April 2021

ABSTRACT
We have studied the developmental appearance of the O-2Aadult progenitor cell, a specific type of oligodendro cyte-type-2 astrocyte (O-2A) progenitor cell that we have identified previously in cultures prepared from the optic nerves of adult rats. O-2Aadult progenitors differ from their counterparts in perinatal animals (O-2Aperina,al progenitor cells) in antigenic phenotype, morphology, cell cycle time, rate of migration, time course of differen tiation into oligodendrocytes or type-2 astrocytes and sensitivity to the lytic effects of complement in vitro. In the present study, we have found that O-2Aadult progeni tor-like cells first appear in the developing optic nerve approximately 7 days after birth and that by 1 month after birth these cells appear to be the dominant progeni tor population in the nerve. Howevér, the perinatal-to-adult transition in progenitor populations is a gradual one and O-2Aadult and O-2Aptrinata progenitors coexist in the optic nerve for 3 weeks or more. In addition, cells derived from optic nerves of P21 rats express character istic features of O-2Aadultand O-2Aptrinata progenitors for extended periods of growth in the same tissue culture dish. Our results thus indicate that the properties that distinguish these two types of O-2A progenitors from each other are expressed in apparently identical environ ments. Thus, these cells must either respond to different signals present in the environment, or must respond with markedly different behaviours to the binding of identical signalling molecules.
Lateral inhibition and cell fate during neurogenesis in Drosophila: the interactions between scute, Notch and Delta
Authors: Cabrera Carlos V. 
Published: April 2021

ABSTRACT
A comparison of the patterns of expression of AS-C (T3) RNA and protein suggests that an important level of regulation occurs post-transcriptionally. First, when the RNA is abundant in the early embryo the protein is barely detectable. Later, the protein starts to accumulate in only a subset of the nuclei of those cells expressing the RNA. Only the cells in the subsets become the neuroblasts. This post-transcriptional regulation is suppressed in embryos mutant for the genes Notch and Delta; where all cells expressing RNA accumulate protein. These findings suggest that deployment of T3 protein expression is one of the causal factors that assigns specific fates to the neuroblasts and, in consequence, a basis for the mechanism of lateral inhibition is proposed.
The Effect of Adenosine Triphosphate and its Decomposition Products on Cortisone Induced Teratology
Authors: Gordon Harry W. , Tkaczyk Walter , Peer Lyndon A. , Bernhard William G. 
Published: April 2021

ABSTRACT
Cortisone has been demonstrated by several investigators to be a teratogenic agent when administered to pregnant mice (Baxter & Fraser, 1950; Fraser & Feinstat, 1951; Ingalls & Curley, 1957; Walker & Fraser, 1957; Gordon et al., 1961). The degree of occurrence was found to vary with strain (Walker & Fraser, 1957; Fraser et al., 1954), maternal age, weight and litter size (Kalter, 1956; 1957).
Malformation of the Extremity in the Mouse Foetus Caused by X-radiation of the Mother During Pregnancy
Authors: Murakami Ujihiro , Kameyama Yoshiro , Nogami Hiroshi 
Published: April 2021

ABSTRACT
Different groups of the ddN strain mice were exposed to X-radiation of 300 r., 200 r. and 150 r. from the 8th to 13th day of pregnancy. In offspring from mothers treated on the 11th day, malformations of the extremities were observed in groups treated with over 200 r. Scapular hypoplasia and shortening of the fore-limb, as a result of absence, synostosis, shortening, flexure or curvature of the limb bone, etc., were typical malformations. However, in the group treated with 150 r. of X-radiations the incidence of such malformations was very low. In offspring from mothers treated on the 12th day, digital reductions, on account of ectrodactylias, were the typical malformation in the fore-limb. Ectrodactylia was dominant in the second digit of the fore-limbs, but involvement of the fifth digit was also seen. In the hind-limbs, the incidence was a little lower and the predominant site of involvement was the third digit. Both in the fore- and hind-limbs, the fourth digit was the most resistant to malformation. Other digital malformations occurred more often in the hind-limb than in the fore-limbs, though not frequently. The formation of ectrodactylias after X-radiation was studied in a follow-up experiment. The process began with cellular necrosis in the hand and foot plate corresponding to the predominant site of ectrodactylias, i.e. chiefly in the second digit of the fore-limb and in the third digit of the hindlimb. The process may damage the precursor of the pre-cartilage. In contrast to the regenerative neural tissue, compensation does not take place in the mesenchymal tissue once the destruction is severe, and the reduction of digits will therefore persist. The effect of X-radiation upon a developing digital primordium may be a directly destructive process. The critical stage for extremity malformations due to thalidomide in human beings corresponds with the critical stage for X-ray malformations of the extremities in mouse.
‘Generic’ physical mechanisms of morphogenesis and pattern formation
Authors: Newman Stuart A. , Comper Wayne D. 
Published: April 2021

Abstract
The role of ‘generic’ physical mechanisms in morphogenesis and pattern formation of tissues is considered. Generic mechanisms are defined as those physical processes that are broadly applicable to living and nonliving systems, such as adhesion, surface tension and gravitational effects, viscosity, phase separation, convection and reaction–diffusion coupling. They are contrasted with ‘genetic’ mechanisms, a term reserved for highly evolved, machine-like, biomolecular processes. Generic mechanisms acting upon living tissues are capable of giving rise to morphogenetic rearrangements of cytoplasmic, tissue and extracellular matrix components, sometimes leading to ‘microfingers’, and to chemical waves or stripes. We suggest that many mor phogenetic and patterning effects are the inevitable outcome of recognized physical properties of tissues, and that generic physical mechanisms that act on these properties are complementary to, and interdependent with genetic mechanisms. We also suggest that major morphological reorganizations in phylogenetic lineages may arise by the action of generic physical mechanisms on developing embryos. Subsequent evolution of genetic mechanisms could stabilize and refine developmental outcomes originally guided by generic effects.
Homologous and heterologous enhancers modulate spatial expression but not cell-type specificity of the murine γF-crystallin promoter
Authors: Yu Calvin C.-K. , Tsui Lap-Chee , Breitman Martin L. 
Published: April 2021

Abstract
Previous studies have shown that mouse γF-crystallin sequences –759 to +45, which include the core promoter and two upstream enhancer elements, contain sufficient information for directing gene expression to terminally differentiated fiber cells of the ocular lens. To investigate the role that proximal sequences of the mouse γF-crystallin promoter play in the developmental regulation of gene expression, we generated transgenic mice containing the lacZ gene driven by either mouse γF-crystallin sequences –171 to +45, which lack functional enhancers, or a hybrid hamster αA-/mouse γF-crystallin promoter, which contains the hamster αA-crystallin enhancer instead of operational γF-crystallin enhancers. In situ analysis of lacZ expression in these mice revealed that the mouse γF-crystallin promoter segment –171 to +45, which shows low activity in vitro, is able to direct gene expression to the fiber cells in the nucleus of the lens. However, animals expressing γ171–lacZ show both a lower level of expression of the lacZ gene and a narrower pattern of staining in the lens nucleus than mice expressing γ759–lacZ, which contains the two enhancer elements located between –392 and –278 and –226 to –123. Moreover, animals expressing the lacZ gene driven by the hybrid αA-/γF-crystallin promoter show a pattern of staining in the lens nucleus similar to that of mice expressing γ759–lacZ, indicating that although the αA-crystallin enhancer is unable to alter the cell-type specificity conferred by the mouse γF-crystallin proximal promoter segment –171 to +45, it is able to expand the spatial domain of gene expression in a manner similar to the native γF-crystallin enhancers. The significance of these results, in terms of the mechanisms governing spatial regulation of gene expression, is discussed.
Expression of the nerve growth factor-regulated NGFI-A and NGFI-B genes in the developing rat
Authors: Watson Mark A. , Milbrandt Jeffrey 
Published: April 2021

Abstract
NGFI-A and NGFI-B are two genes that are induced in PC 12 cells treated with nerve growth factor and encode zinc-finger proteins that may act as transcription factors. To study the function of these genes in vivo, their expression in rat embryos and postnatally developing tissues was examined. Both genes are expressed during embryogenesis from E12 to E18. In postnatally developing animals, these genes are induced in cortex, midbrain and cerebellum, suggesting that they may function in one or many of the changes that occur during postnatal maturation of the brain. Both genes are expressed at a low, constitutive level in a subset of other non-neuronal tissues, but also demonstrate developmental changes in expression in many other organs. To examine expression of these genes in ganglia of the peripheral nervous system, a sensitive and quantitative assay employing reverse transcription and polymerase chain reaction was developed. Results obtained with this assay demonstrated that expression of both NGFI-A and NGFI-B is modulated in the peripheral nervous system during postnatal maturation, but not in a pattern concordant with previously characterized NGF receptor expression. These studies suggest that NGFI-A and NGFI-B serve multiple, tissue-specific functions and are under complex regulation in vivo.