bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunological, biochemical and physiological analyses of cardioacceleratory peptide 2 (CAP2) activity in the embryo of the tobacco hawkmoth Manduca sexta
Authors: Broadie Kendal S. , Sylwester Andrew W. , Bate Michael , Tublitz Nathan J. 
Published: April 2021

ABSTRACT
The cells In the embryonic CNS of the tobacco hawkmoth, Manduca sexta, that synthesize a cardioacceleratory peptide 2 (CAP2)-llke antigen were identified using immunohistochemical techniques. Two distinct neurosecretory cell types were present in the abdominal ventral nerve cord (VNC) that contain CAP2-like immunoreactivity during late embryogenesis: a pair of large (diameter range 15–20 μm) cells lying along the posterior, dorsal midline of abdominal ganglia A4–A8, and a bilateral set of four smaller (diameter range 6–11 μm) neurons which lie at the base of each ventral root in abdominal ganglia A2–A8. CAP2-like accumulation appeared to follow independent patterns in the two cell types. CAP2-like immunoreactivity began at 60% of embryo development (DT) in the medial cells, accumulated steadily throughout embryogenesis, and dropped markedly during hatching. Lateral cells synthesized the CAP2-like antigen later in development (70 % DT) and showed a sharp drop in antigen levels between 75 % and 80 % of embryonic development.
Extracts from developing M. sexta embryos were found to contain a cardioactive factor capable of accelerating the contraction frequency of the pharate adult moth heart in a fashion similar to CAP2. Immunoprecipitation with a monoclonal antibody that specifically recognizes the two endogenous Manduca cardioacceleratory peptides and purification using high pressure liquid chromatography identified this factor as cardioac-celeratory peptide 2 (CAP2). Using an in vitro heart bioassay, the levels of this cardioactive neuropeptide were traced during the development of the M. sexta embryo. As with the immunohistochemical results, two periods during embryogenesis were identified in which the level of CAP2 dropped markedly: between 75 % and 80 % development, and at hatching. Embryo bioassays of CAP2 activity were used to identify possible target tissues for physiological activity during these two putative release times. CAP2 was found to accelerate contraction frequency in the embryonic heart and hindgut of Manduca in a dose-dependent fashion. Of these two possible targets, the hindgut proved to be more sensitive to CAP2, having a lower response threshold and a longer duration of response to a given concentration of the exogenously applied peptide.
Based on these immunocytochemical, pharmacological and biochemical results, and on a previously published detailed analysis of Manduca embryogenesis, we conclude that CAP2 is probably released from a specific set of identified neurosecretory cells in the abdominal VNC to modulate embryonic gut activity at 75–80 % of embryo development during ingestion of the extra-embryonic yolk.
Spatial and temporal patterns of neurogenesis in the embryo of the locust (Schistocerca gregaria)
Authors: Shepherd D. , Bate C. M. 
Published: April 2021

ABSTRACT
Embryonic neurogenesis in the ventral nerve cord of the locust Schistocerca gregaria was studied using toluidine blue (TB) staining and birthdating of cells by incorporation of bromodeoxyuridine (BUdR). In the thorax, the neuroblasts (NBs) start dividing at the 28 % stage and neurogenesis continues until 90%. In the abdomen, neurogenesis starts at about 30 % and continues until 70 %. Every NB appears to have its own fixed period of division before disappearing. Thus a specific spatial and temporal pattern of NB degeneration can be seen in every segment. This pattern is identical in each of the three thoracic ganglia. We have traced the fate of each of the original complement of NBs in the mesothoracic neuromere and specified the stage of development at which each NB ends its lineage and disappears. The abdominal segments A2 to A7 share an identical pattern of NB death, which is not comparable to the thoracic pattern. The progress of neurogenesis is marked by a gradual decrease in the number of NBs, with NBs in the thoracic ganglia persisting longer than their abdominal homologues. The differences between the thoracic and abdominal NBs are also reflected in the rates at which they divide, thoracic NBs dividing at almost twice the rate of the abdominal NBs.
Specific spatial and temporal distribution of retinoic acid receptor gamma transcripts during mouse embryogenesis
Authors: Ruberte Esther , Dolle Pascal , Krust Andree , Zelent Arthur , Morriss-Kay Gillian , Chambon Pierre 
Published: April 2021

Abstract
Retinoic acid (RA), a putative morphogen in vertebrates, has profound effects on development during embryogenesis, chondrogenesis and differentiation of squamous epithelia. The distribution of the transcripts of the retinoic acid receptor gamma (RAR-γ) gene has been studied here by in situ hybridization during mouse development from days 6.5 to 15.5 post-coitum (p.c.). RAR-γ transcripts are detected as early as day 8 p.c. in the presomitic posterior region. Between days 9.5 and 11.5 p.c., the transcripts are uniformly distributed in the mesenchyme of the frontonasal region, pharyngeal arches, limb buds and sclerotomes. At day 12.5 p.c., RAR-γ transcripts are found in all precartilaginous mesenchymal condensations. From day 13.5 p.c., the transcripts are specifically localized in all cartilages and differentiating squamous keratinizing epithelia, irrespective of their embryological origin. RAR-γ transcripts are also found in the developing teeth and whisker follicles. The developmental pattern of expression of the RAR-γ gene suggests that RAR-γ plays a crucial role for transducing RA signals at the level of gene expression during morphogenesis, chondrogenesis and differentiation of squamous epithelia.
Transition of myosin isozymes during development of human masseter muscle: Persistence of developmental Isoforms during postnatal stage
Authors: Soussi-Yanicostas N. , Barbet J. P. , Laurent-Winter C. , Barton P. , Butler-Browne G. S. 
Published: April 2021

Abstract
Previous results have shown that the adult human masseter muscle contains myosin isoforms that are specific to early stages of development in trunk and limb muscles, i.e. embryonic and fetal (neonatal) myosin heavy chains (MHC) and embryonic myosin light chain (MLC1emb). We wanted to know if this specific pattern is the result of a late maturation or of a distinct evolution during development.
We show here that the embryonic and the fetal MHC and the MLC1emb are expressed throughout perinatal and postnatal masseter development. Our results also demonstrate that MLC1emb accumulation increases considerably during the postnatal period. In addition, both the slow MLCs and the slow isoform of tropomyosin are expressed later in the masseter than quadriceps and the fast skeletal muscle isoform MLC3 is not detected during fetal and early postnatal development in the masseter whereas it is expressed throughout fetal development in the quadriceps.
Our results thus confirm previous histochemical data and demonstrate that the masseter muscle displays a pattern of myosin and tropomyosin isoform transitions different to that previously described in trunk and limb muscles. This suggests that control of masseter muscle development involves mechanisms distinct from other body muscles, possibly as a result of either its craniofacial innervation or of a possibly different embryonic origin.
Developmental expression of the putative transcription factor Egr-1 suggests that Egr-1 and c-fos are coregulated in some tissues
Authors: Mcmahon Andrew P. , Champion Janet E. , Mcmahon Jill A. , Sukhatme Vikas P. 
Published: April 2021

Abstract
We have investigated developmental expression of the gene Egr-1, which encodes a protein containing three zinc fingers. Egr-1 like c-fos is a serum inducible, early response gene, which is co-induced with c-fos in a variety of quite different situations. A single 3.7-kb RNA was detected throughout fetal mouse development, which increased in absolute levels in total fetal RNA from 9.5 to 12.5 days post coitum (p.c.). In situ hybridization to 14.5- and 17.5-day p.c. fetal tissues demonstrated Egr-1 accumulation at several specific sites. These included mesenchymal components of the developing tooth germs and salivary and nasal glands; an ectodermally derived component of the whisker pad and developing muscle, cartilage, and bone. Expression of Egr-1 in cartilage and bone showed a strikingly similar expression to previously published reports of c-fos in these tissues. High levels of Egr-1 RNA was observed at the perichondrial interface of opposing cartilaginous elements and in interstitial cells that lie in between. Bone expression was observed in membranous bone of the head, alveolar bone around the tooth germs, and at periosteal and endochondral ossification sites in the limb bones. Our data support the idea that Egr-1 and c-fos may be coregulated in vivo and together may regulate normal development of the skeleton.
The role of the dorsal lip in the induction of heart mesoderm in Xenopus laevis
Authors: Sater Amy K. , Jacobson Antone G. 
Published: April 2021

Abstract
We have examined the tissue interactions responsible for the expression of heart-forming potency during gastrulation. By comparing the specification of different regions of the marginal zone, we show that heart-forming potency is expressed only in explants containing both the dorsal lip of the blastopore and deep mesoderm between 30° and 45° lateral to the dorsal midline. Embryos from which both of these 30°-45° dorsolateral regions have been removed undergo heart formation in two thirds of cases, as long as the dorsal lip is left intact. If the dorsal lip is removed along with the 30° – 45° regions, heart formation does not occur. These results indicate that the dorsolateral deep mesoderm must interact with the dorsal lip in order to express heart-forming potency. Transplantation of the dorsal lip into the ventral marginal zone of host embryos results in the formation of a secondary axis; in over half of cases, this secondary axis includes a heart derived from the host mesoderm. These findings suggest that the establishment of heart mesoderm is initiated by a dorsalizing signal from the dorsal lip of the blastopore.
Pathways of trunk neural crest cell migration in the mouse embryo as revealed by vital dye labelling
Authors: Serbedzija George N. , Fraser Scott E. , Bronner-Fraser Marianne 
Published: April 2021

Abstract
Analysis of neural crest cell migration in the mouse has been difficult due to the lack of reliable cell markers. Recently, we found that injection of Dil into the chick neural tube marks premigratory neural crest cells whose endfeet are in contact with the lumen of the neural tube (Serbedzija et al. Development 106, 809-819 (1989)). In the present study, this technique was applied to study neural crest cell migratory pathways in the trunk of the mouse embryo. Embryos were removed from the mother between the 8th and the 10th days of development and Dil was injected into the lumen of the neural tube. The embryos were then cultured for 12 to 24 h, and analyzed at the level of the forelimb. We observed two predominant pathways of neural crest cell migration: (1) a ventral pathway through the rostral portion of the somite and (2) a dorsolateral pathway between the dermamyotome and the epidermis. Neural crest cells were observed along the dorsolateral pathway throughout the period of migration. The distribution of labelled cells along the ventral pathway suggested that there were two overlapping phases of migration. An early ventrolateral phase began before E9 and ended by E9.5; this pathway consisted of a stream of cells within the rostral sclerotome, adjacent to the dermamyotome, that extended ventrally to the region of the sympathetic ganglia and the dorsal aorta. A later ventromedial phase was apparent after E9.5 and continued through E10.5; this pathway consisted of a thin strand of Dil-labelled cells along the lateral surface of the neural tube which later protruded into the rostral sclerotome to form the dorsal root ganglia and Schwann cells. Those embryos injected at later stages contained labelled cells only in dorsal derivatives, suggesting that neural crest derivatives are populated in a ventral-to-dorsal order. While the overall pattern and order of neural crest migration was similar to that previously observed in avians and rats, some details of the timing and trajectories apparently differed, most notably the timing of neural crest migration along the dorsolateral pathway.
The role of gap junctions in patterning of the chick limb bud
Authors: Allen Francesca , Tickle Cheryll , Warner Anne 
Published: April 2021

Abstract
The role of gap junctional communication during patterning of the chick limb has been investigated. Affinity-purified antibodies raised against rat liver gap junctional proteins were used to block communication between limb mesenchyme cells. Co-injection of the antibodies and Lucifer yellow Into mesenchyme cultures demonstrated that communication was inhibited almost immediately. When antibodies were loaded into mesenchyme tissue by DMSO permeabilisation, [3H]nucleotide transfer was prevented for at least 16 h.
Polarising region tissue from the posterior limb bud margin causes digit duplications when grafted to the anterior margin. Quail polarising region cells were loaded with gap junction antibody and grafted into chick wing buds. The antibody had no effect on growth or survival of the grafted cells. As very few polarising region cells are required to initiate duplications, the number of polarising region cells in the grafts was reduced by diluting 1:9 with anterior mesenchyme tissue.
When either polarising region or anterior mesenchyme tissue in the graft was loaded separately with antibody, there was little effect on respecification of the digit pattern. However, loading both tissues in the graft caused a significant decrease in duplications. This indicates that a major role of gap junctions in limb patterning may be to enable polarising region cells to communicate directly with adjacent anterior mesenchyme. A role for gap junctional communication between anterior mesenchyme cells cannot be excluded. The results are discussed in relation to the role of retinoic acid as a putative morphogen.
Thyroxine-dependent modulations of the expression of the neural cell adhesion molecule N-CAM during Xenopus laevis metamorphosis
Authors: Levi Giovanni , Broders Florence , Dunon Dominique , Edelman Gerald M. , Thiery Jean Paul 
Published: April 2021

Abstract
During amphibian metamorphosis, a complete remodeling of the phenotype takes place under complex hormonal control whose final effectors are thyroid hormones. This process implies the activation of coordinated programs of cell death, proliferation, migration, adhesion and differentiation. Inasmuch as the neural cell adhesion molecule N-CAM is thought to play a central role in the control of morphogenetic processes, we have studied by immunohistofluorescence and immunoblots the patterns of expression of N-CAM at different stages of Xenopus laevis metamorphosis. A scan was made of all major organs and appendages.
Before the metamorphic climax, all neuronal cell bodies and processes express high levels of N-CAM. During the metamorphic climax, N-CAM expression decreases sharply on the cell bodies and processes of the peripheral nervous system (PNS) but remains high in the central nervous system (CNS). Towards the end of metamorphosis, the PNS and spinal nerves are virtually negative for N-CAM while the CNS is still positive. The optic and olfactory nerves, although myelinated, are still strongly positive for N-CAM. The lens and olfactory epithelia express N-CAM throughout metamorphosis. In the brain, N-CAM is present at all times as three polypeptides of 180, 140, and 120X103Mr; before metamorphosis some of the N-CAM is in its polysialylated form. During metamorphosis and the subsequent growth of the animal, the amount of N-CAM decreases gradually. In all polypeptides, the polysialylated form is the first to disappear.
Cardiac muscle expresses high level of N-CAM from its first formation throughout metamorphosis; in contrast, the level of N-CAM in skeletal muscle is high in newly formed muscles, but decreases rapidly after myoblast fusion.
The liver of adult Xenopus contains large amounts of a 160 xlO3 polypeptide that is recognized by polyclonal and monoclonal antibodies against N-CAM. cDNA probes of Xenopus brain N-CAM recognize major transcripts of 9.2, 3.8 and 3.3 kb in Xenopus liver mRNA; these bands are different in size from those recognized in brain mRNA (9.5, 4.2 and 2.2 kb).
Premetamorphic liver does not express the 160xlO3 form of N-CAM, which can be first detected at stage 59 and persists then through all the life of the animal. Expression of N-CAM in the liver can be induced in premetamorphic animals (stage 51-52) by a 48 h treatment with thyroxine. All hepatocytes are responsive.
The thyroxine-dependent induction of the expression of N-CAM in the liver provides the first example of hormonally induced expression of a cell adhesion molecule. These results are discussed in terms of the potential morphogenetic roles of the various forms of N-CAM in development and metamorphosis.
How imprinting is relevant to human disease
Authors: Hall Judith G. 
Published: April 2021

ABSTRACT
Genomic imprinting appears to be a ubiquitous process in mammals involving many chromosome segments whose affects are dependent on their parental origin. One of the challenges for clinical geneticists is to determine which disorders are manifesting imprinting effects and which families are affected. Re-evaluation of cases of chromosomal abnormalities and family histories of disease manifestations should give important clues. Examination of the regions of human chromosomes homologous to mouse imprinted chromosomal regions may yield useful information. Cases of discordance in monozygous twins may also provide important insights into imprinted modification of diseases.
Variation and inheritance of cytosine methylation patterns in wheat at the high molecular weight glutenin and ribosomal RNA gene loci
Authors: Flavell R. B. , O’Dell M. 
Published: April 2021

ABSTRACT
Chromosome marking by cytosine methylation has been examined in two gene systems in wheat - at the loci encoding high molecular weight (BMW) glutenin sub-units (seed proteins) and ribosomal RNA. Variation in cytosine methylation occurs between progeny in highly inbred lines around the BMW glutenin locus. The variation is inherited through meiosis to F1 and F2 generations but occasionally a new variant arises. Specific cytosine residues lose their methyl group in the seed, the organ where the genes are expressed.
Within the multigene family of ribosomal RNA genes, several subsets of genes can be defined based upon the cytosine methylation patterns. High activity of a ribosomal RNA gene locus is correlated with loss of methylation at specific cytosine residues, especially in the promoter and upstream regulatory regions. A model is described in which the subset of genes selected to be used are those to which specific regulatory proteins and transcription complexes bind most favourably. Binding of such proteins inhibits cytosine methylation and so marks the subset of genes for expression in subsequent cell generations. Examples are described where new types of RNA genes are introduced via sexual crosses that result in changes to the methylation patterns of the ribosomal RNA genes. The processes determining the changes begin, it is believed, in the fertilised egg.
Autosomal and X-chromosome imprinting
Authors: Cattanach Bruce M. , Beechey Colin V. 
Published: April 2021

ABSTRACT
Mouse genetic studies using Robertsonian and reciprocal translocations have shown that certain autosomal regions of loci are subject to a parental germ line imprint, which renders maternal and paternal copies functionally inequivalent in the embryo or later stages of development. Duplication of maternal or paternal copies with corresponding paternal/maternal deficiencies in chromosomally balanced zygotes causes various effects. These range from early embryonic lethalities through to mid-fetal and neonatal lethalities, and in some instances viable young with phenotypic effects are obtained. Eight to nine chromosomal regions that give such imprinting effects have been identified. Six to seven of these regions are located in only three chromosomes (2, 7 and 17). The two other regions are located in chromosomes 6 and 11. Maternal and paternal disomies for each of four other chromosomes (1, 5, 9 and 14) have been recovered with different frequencies, but the possibility that this may be due to imprinting has yet to be supported by follow-up studies on regions of the chromosomes concerned. No clear evidence of genetic-background modifications of the imprinting process have been observed in these mouse genetic experiments.
The mammalian X chromosome is also subject to imprinting, as demonstrated by the non-random, paternal X-inactivation in female mouse extra-embryonic tissues and in the somatic cells of marsupial females. There is also the opposite bias towards inactivation of the maternal X in the somatic cells of female mice. On the basis that both X-chromosome inactivation and autosomal chromosome imprinting may be concerned with gene regulation, it is suggested that evidence from X-chromosome inactivation studies may help to elucidate factors underlying the imprinting of autosomes. The relevant aspects of X-inactivation are summarized.
The DDK inbred strain as a model for the study of interactions between parental genomes and egg cytoplasm in mouse preimplantation development
Authors: Babinet Charles , Richoux Véronique , Guénet Jean-Louis , Renard Jean-Paul 
Published: April 2021

ABSTRACT
The DDK strain of mice has unusual genetic properties. When females of this strain are crossed to males of other strains, they generally exhibit a very low fertility, whereas reciprocal crosses are fully fertile as are the intrastrain crosses. The observed low fertility results from early embryonic lethality, the F1 embryos dying around the late morula-early blastocyst stage. Nuclear transplantation experiments between hybrid eggs of BALB/c and DDK strains has shown that failure of F1 (DDK♀ × BALB/CC♂) embryos to develop is not due to the combination per se of maternal (DDK) and paternal (BALB/c) genomes but rather to an incompatibility between paternal (BALB/c) genomic contribution and DDK cytoplasm. This incompatibility does not occur between a female BALB/c pronucleus and the DDK cytoplasm, suggesting the involvement of a differential imprinting of parental genomes. Introduction of cytoplasts isolated from DDK 1- to 8-cell embryos into BALB/c♀ xBALB/c♂ or BALB/c♀ xDDK♂ embryos of the corresponding developmental stage demonstrate that the cytoplasm of DDK embryos prevents the formation of normal blastocysts through a specific interaction with the paternal component of the BALB/c diploid nucleus. Genetic and molecular studies are underway to try and isolate the gene(s) responsible for the failure of (DDK♀ BALB/C♂)F1 embryos. These experiments should help in our understanding of nucleocytoplasmic interactions and the respective roles of parental genomes in early embryonic development.