bluuebunny/crossref_metadata_2025_split huggingface dataset:
Brachyury - a gene affecting mouse gastrulation and early organogenesis
Authors: Beddington R. S. P. , Rashbass P. , Wilson V. 
Published: April 2021

ABSTRACT
Mouse embryos that are homozygous for the Brachyury (T) deletion die at mid-gestation. They have prominent defects in the notochord, the allantois and the primitive streak. Expression of the T gene commences at the onset of gastrulation and is restricted to the primitive streak, mesoderm emerging from the streak, the head process and the notochord. Genetic evidence has suggested that there may be an increasing demand for T gene function along the rostrocaudal axis. Experiments reported here indicate that this may not be the case. Instead, the gradient in severity of the T defect may be caused by defective mesoderm cell movements, which result in a progressive accumulation of mesoderm cells near the primitive streak.
Embryonic stem (ES) cells which are homozygous for the T deletion have been isolated and their differentiation in vitro and in vivo compared with that of heterozygous and wild-type ES cell lines. In +/+ ↔ T/T ES cell chimeras the Brachyury phenotype is not rescued by the presence of wild-type cells and high level chimeras show most of the features characteristic of intact T/T mutants. A few offspring from blastocysts injected with T/T ES cells have been born, several of which had greatly reduced or abnormal tails. However, little or no ES cell contribution was detectable in these animals, either as coat colour pigmentation or by isozyme analysis. Inspection of potential +/+ ↔ T/T ES cell chimeras on the 11th or 12th day of gestation, stages later than that at which intact T/T mutants die, revealed the presence of chimeras with caudal defects. These chimeras displayed a gradient of ES cell colonisation along the rostrocaudal axis with increased colonisation of caudal regions. In addition, the extent of chimerism in ectodermal tissues (which do not invaginate during gastrulation) tended to be higher than that in mesodermal tissues (which are derived from cells invaginating through the primitive streak). These results suggest that nascent mesoderm cells lacking the T gene are compromised in their ability to move away from the primitive streak. This indicates that one function of the T gene may be to regulate cell adhesion or cell motility properties in mesoderm cells. Wild-type cells in +/+ ↔ T/T chimeras appear to move normally to populate trunk and head mesoderm, suggesting that the reduced motility in T/T cells is a cell autonomous defect
Dorsoventral development of the Drosophila embryo is controlled by a cascade of transcriptional regulators
Authors: Thisse Christine , Thisse Bernard 
Published: April 2021

ABSTRACT
Maternal genes involved in dorsoventral (D/V) patterning of the Drosophila embryo interact to establish a stable nuclear concentration gradient of the Dorsal protein which acts as the morphogen along this axis. This protein belongs to the rel proto-oncogene and NF-KB transcriptional factor family and acts by controlling zygotic gene expression. In the ventral part of the embryo, dorsal specifically activates transcription of the gene twist and ventrally and laterally dorsal represses the expression of zerkn üllt, a gene involved in the formation of dorsal derivatives. The extent of dorsal action is closely related to the affinity and the number of dorsal response elements present in these zygotic gene promoters.
twist is one of the first zygotic genes necessary for mesoderm formation. It codes for a ‘b-HLH’ DNA-bind-ing protein which can dimerize and bind to DNA in vitro and to polytene chromosomes in vivo. In addition, in cultured cells twist has been shown to be a transcriptional activator. Thus, the first events of embryonic development along the D/V axis are controlled at the transcriptional level.
A gastrulation center in the ascidian egg
Authors: Jeffery William R. 
Published: April 2021

ABSTRACT
A gastrulation center is described in ascidian eggs. Extensive cytoplasmic rearrangements occur in ascidian eggs between fertilization and first cleavage. During ooplasmic segregation, a specific cytoskeletal domain (the myoplasm) is translocated first to the vegetal pole (VP) and then to the posterior region of the zygote. A few hours later, gastrulation is initiated by invagination of endoderm cells in the VP region of the 110-cell embryo. After the completion of gastrulation, the embryonic axis is formed, which includes induction of the nervous system, morphogenesis of the larval tail and differentiation of tail muscle cells. Microsurgical deletion or ultraviolet (UV) irradiation of the VP region during the first phase of myoplasmic segregation prevents gastrulation, nervous system induction and tail formation, without affecting muscle cell differentiation. Similar manipulations of unfertilized eggs or uncleaved zygotes after the second phase of segregation have no effect on development, suggesting that a gastrulation center is established by transient localization of myoplasm in the VP region. The function of the gastrulation center was investigated by comparing protein synthesis in normal and UV-irradiated embryos. About 5% of 433 labelled polypeptides detected in 2D gels were affected by UV irradiation. The most prominent protein is a 30 kDa cytoskeletal component (p30), whose synthesis is abolished by UV irradiation. p30 synthesis peaks during gastrulation, is affected by the same UV dose and has the same UV-sensitivity period as gastrulation. However, p30 is not a UV-sensitive target because it is absent during ooplasmic segregation, the UV-sensitivity period. Moreover, the UV target has the absorption maximum of a nucleic acid rather than a protein. Cell-free translation studies indicate that p30 is encoded by a maternal mRNA. UV irradiation inhibits the ability of this transcript to direct p30 synthesis, indicating that p30 mRNA is a UV-sensitive target The gastrulation center may function by sequestration or activation of maternal mRNAs encoding proteins that function during embryogenesis.
Differential expression of the HMG box factors TCF-1 and LEF-1 during murine embryogenesis
Authors: Oosterwegel Mariëtte , van de Wetering Marc , Timmerman Janneke , Kruisbeek Ada , Destree Olivier , Meijlink Frits , Clevers Hans 
Published: April 2021

ABSTRACT
The recent identification of a number of T lymphocytespecific enhancers has allowed the cloning of several novel transcription factors. Two of these, TCF-1 and LEF-1, contain a virtually identical DNA-binding domain of the High Mobility Group (HMG-1) box type. TCF-1 and LEF-1 originate from a recent gene duplication event as evidenced by comparison with the chicken homologue, chTCF. We have now analyzed the differential expression of these two transcription factors. In a panel of lymphoid cell lines, TCF-1 was exclusively expressed in the T cell lineage. In contrast, LEF-1 mRNA was detected at equivalent levels in proand pre-B cells and in all T lineage cells.
In situ hybridization on murine embryos revealed that TCF-1 and LEF-1 were widely expressed at day 7.5 of gestation. At later stages, the expression patterns were complex and only partially overlapping. The expression of TCF-1 and LEF-1 coincided until day 10.5, when mRNAs were detected in limb buds, neural crest, pharyngeal arches and nasal process. At later time points (day 13.5 to 14.5), sites of overlapping expression included lung, the urogenital system, tooth buds, thymus and choroid plexus. Unique expression sites for TCF-1 included Reichert’s membrane and trophectodermderived cells, the ribs and thoracic prevertebrae, craniofacial structures, the adrenal gland and meninges. Unique LEF-1 expression was observed in the tail prevertebrae, brain and inner ear. Postnatally, expression of both genes could only be detected in lymphoid tissues. These observations suggest that TCF-1 and LEF-1 exert differential functions during murine embryogenesis.
Size regulation and morphogenesis: a cellular analysis of skeletogenesis in the sea urchin embryo
Authors: Ettensohn Charles A. , Malinda Katherine M. 
Published: April 2021

ABSTRACT
The formation of the skeleton is a central event in sea urchin morphogenesis. The skeleton serves as a framework for the larval body and is the primary determinant of its shape. Previous studies have shown that the size of the skeleton is invariant despite wide experimentally induced variations in the number of skeleton forming primary mesenchyme cells (PMCs). In the present study, we have used PMC transplantation, fluorescent cell markers and confocal laser scanning microscopy to analyze cellular aspects of skeletal patterning. Labeling of embryos with 5-bromodeoxyuridine demonstrates that the entire embryonic phase of skeletal morphogenesis occurs in the absence of PMC division. During embryogenesis, skeletal rods elongate by one of two mechanisms; either preceded by a cluster (plug) of PMCs or by extending along an existing PMC filopodial cable. Elongation of skeletal rods occurs exclusively by the addition of new material at the rod tips, although radial growth (increase in rod thickness) occurs along the length of the rods. Photoablation of a distinctive region of ectoderm cells at the arm tip results in an inhibition of skeletal rod elongation, indicating that a local ectoderm-PMC interaction is required for skeletal growth. The regulation of skeletal patterning was also examined in embryos that had been microinjected with additional PMCs and in half-sized larvae derived from blastomeres isolated at the 2-cell stage. Microinjection of 50-100 PMCs into the blastocoel at the mesenchyme blastula stage leads to an increase in the numbers of PMCs along all skeletal rods and a two-fold increase in the number of cells in the plugs, yet no increase in the length of the skeletal rods. The length of the anal rods can, however, be increased by microinjecting developmentally ‘young’ PMCs into the arm tips of late stage embryos. We find that the rate of skeletal rod elongation is independent of both the mode of rod growth (chain or plug) and the number of PMCs in the plug at the growing rod tip. Instead, the rate of elongation appears to be strictly regulated by the quantity of ectodermal tissue present in the embryo. These studies provide new information concerning normal mechanisms of skeletal growth and patterning and lead us to propose a model for the regulation of skeleton size based upon an intrinsic PMC ‘clock’ and an ectoderm-derived signal that regulates the rate of skeletal rod elongation.
The regulation and function of the helix-loop-helix gene, asense, in Drosophila neural precursors
Authors: Jarman Andrew P. , Brand Michael , Jan Lily Y. , Jan Yuh Nung 
Published: April 2021

ABSTRACT
asense is a member of the achaete-scute complex (AS-C) of helix-loop-helix genes involved in Drosophila neurogenesis. Unlike the other AS-C members, which are expressed in subsets of the ectodermal areas (proneural clusters) that give rise to neural precursors, asense is one of a number of genes that are specifically expressed in the neural precursors themselves (the neural precursor genes). We have identified a mutant asense phenotype that may reflect this later expression pattern. As a step in understanding the determination of neural precursors from the proneural clusters, we have investigated the potential role of the AS-C products as direct transcriptional activators of neural precursor genes by analysing the regulation of asense. Using genomic rescues and asense-lacZ fusion genes, the neural precursor regulatory element has been identified. We show that this element contains binding sites for AS-C/daughterless heterodimers. Deletion of these sites reduces the expression from the fusion gene, but significant expression is still achieved, pointing to the existence of other regulators of asense in addition to the AS-C. asense differs from the other AS-C members in its expression pattern, regulation, mutant phenotype and some DNA-binding properties.
Control of flower development in Arabidopsis thaliana by APETALA1 and interacting genes
Authors: Bowman John L. , Alvarez John , Weigel Detlef , Meyerowitz Elliot M. , Smyth David R. 
Published: April 2021

ABSTRACT
Mutations in the APETALA1 gene disturb two phases of flower development, flower meristem specification and floral organ specification. These effects become manifest as a partial conversion of flowers into inflorescence shoots and a disruption of sepal and petal development. We describe the changes in an allelic series of nine apetala1 mutants and show that the two functions of APETALA1 are separable. We have also studied the interaction between APETALA1 and other floral genes by examining the phenotypes of multiply mutant plants and by in situ hybridization using probes for several floral control genes. The results suggest that the products of APETALA1 and another gene, LEAFY, are required to ensure that primordia arising on the flanks of the inflorescence apex adopt a floral fate, as opposed to becoming an inflorescence shoot. APETALA1 and LEAFY have distinct as well as overlapping functions and they appear to reinforce each other’s action. CAU - LIFLOWER is a newly discovered gene which positively regulates both APETALA1 and LEAFY expression. All functions of CAULIFLOWER are redundant with those of APETALA1. APETALA2 also has an early function in reinforcing the action of APETALA1 and LEAFY, especially if the activity of either is compromised by mutation. After the identity of a flower primordium is specified, APETALA1 interacts with APETALA2 in controlling the development of the outer two whorls of floral organs.
The expression of a zebrafish gene homologous to Drosophila snail suggests a conserved function in invertebrate and vertebrate gastrulation
Authors: Hammerschmidt Matthias , Nüsslein-Volhard Christiane 
Published: April 2021

ABSTRACT
Snail, a zinc finger protein, is required for the formation of the ventral furrow and the mesoderm during gastrulation of the Drosophila embryo. snail homologues have been cloned from Xenopus and mouse. We have isolated a zebrafish homologue of snail, designated sna-1. Like its Drosophila counterpart, Sna-1 protein is nuclear. Maternal and zygotic sna-1 transcripts are ubiquitously distributed in zebrafish embryos of cleavage and blastula stages. In gastrulating embryos, sna-1 is expressed in involuting cells of the germ ring, but not in those at the dorsal midline, the presumptive notochordal region. After involution, the expression is maintained in the paraxial mesoderm and becomes prominent in the muscle pioneer precursors, followed by expression at the posterior somite boundaries. Later, sna-1 is expressed in neural crest and mesodermal derivatives of the head region. Sna-1 expression is induced in animal cap cells by activin A. The early sna-1 expression pattern in gastrulating zebrafish no tail (ntl) mutant embryos is normal except a reduction in the level of sna-1 transcription, suggesting that Ntl protein is not the key activator of sna-1 transcription in vivo, but might be involved in the enhancement or maintenance of sna-1 transcription. Data obtained in studies with ectopic ntl expression support this model.
Variable and multiple expression of Protease Nexin-1 during mouse organogenesis and nervous system development
Authors: Mansuy Isabelle M. , van der Putten Herman , Schmid Peter , Meins Marita , Botteri Florence M. , Monard Denis 
Published: April 2021

ABSTRACT
Protease Nexin-1 (PN-1) also known as Glia-Derived Nexin (GDN) inhibits the activity of several serine proteases including thrombin, tissue (tPA)and urokinase (uPA)-type plasminogen activators. These and other serine proteases seem to play roles in development and tissue homeostasis. To gain insight into where and when PN-1 might counteract serine protease activities in vivo, we examined its mRNA and protein expression in the mouse embryo, postnatal developing nervous system and adult tissues. These analyses revealed distinct temporal and spatial PN-1 expression patterns in developing cartilage, lung, skin, urogenital tract, and central and peripheral nervous system. In the embryonic spinal cord, PN-1 expression occurs in cells lining the neural canal that are different from the cells previously shown to express tPA. In the developing postnatal brain, PN-1 expression appears transiently in many neuronal cell populations. These findings suggest a role for PN-1 in the maturation of the central nervous system, a phase that is accompanied by the appearance of different forms of PN-1. In adults, few distinct neuronal cell populations like pyramidal cells of the layer V in the neocortex retained detectable levels of PN-1 expression. Also, mRNA and protein levels did not correspond in adult spleen and muscle tissues. The widespread and complex regulation of PN-1 expression during embryonic development and, in particular, in the early postnatal nervous system as well as in adult tissues suggests multiple roles for this serine protease inhibitor in organogenesis and tissue homeostasis.
Differential expression of neurotrophin receptors during renal development
Authors: Durbeej Madeleine , Söderström Stine , Ebendal Ted , Birchmeier Carmen , Ekblom Peter 
Published: April 2021

ABSTRACT
Early kidney differentiation is driven by local cell-cell interactions. The metanephrogenic mesenchyme stimulates the epithelial ureter bud to grow and branch, whereas the ureter bud stimulates the mesenchyme to convert into a new epithelium. These interactions may be dependent on local growth factors and their receptors. We studied the expression of receptors for nerve growth factors during kidney development. Expression of the lowand high-affinity receptors was cell-type specific. The low-affinity NGF receptor was found in the uninduced mesenchyme at early developmental stages, but in the glomerular podocytes at later developmental stages. In contrast, the high-affinity trkB receptor was found in the cortical mesenchyme cells that will differentiate into stroma. The trkC receptor was found only weakly expressed and in a few parts of the collecting ducts. The role of these receptors and c-ros, a receptor-type kinase expressed on the tip of the ureter bud, was studied by modified antisense oligonucleotides. However, we found that both sense, antisense and nonsense phosphorothioate oligonucleotides inhibited mouse and rat embryonic kidney development in vitro. The oligonucleotides appeared to be toxic for rodent embryonic kidneys in the experimental conditions that we used. Moreover, oligonucleotides did not penetrate well into the epithelial sheets in the organ cultures. We conclude that studies with phosphorothioate antisense oligonucleotides in organ cultures of embryonic kidneys should be interpreted with caution. Our current data do not allow us to not assign a function for the lowor highaffinity NGF receptors or c-ros in kidney development.
A dual requirement for neurogenic genes in Drosophila myogenesis
Authors: Bate Michael , Rushton Emma , Frasch Manfred 
Published: April 2021

ABSTRACT
In wild-type embryos of Drosophila melanogaster, the formation of differentiated larval muscles is preceded by the segregation of small numbers of progenitor or founder cells in the embryonic mesoderm. The founder cells, characterised by the expression of genes encoding putative transcription factors such as S59 or vestigial, fuse with neighbouring myoblasts to form syncytial precursors of individual muscles. Founder cell segregation is deranged in embryos mutant for any of the neurogenic genes: enlarged clusters of cells expressing S59 or vestigial are detected at the sites where small numbers of founder cells segregate in the wild type. In addition, muscle differentiation is deranged in such embryos in a way that appears to be closely linked to the extent of epidermal disruption caused by the neurogenic phenotype: myoblast fusion is limited to regions of the mesoderm beneath the residual epidermis left by the hyperplasia of the nervous system, and late expression of S59 and vestigial is lost from mesoderm not lying within the margins of the residual epidermis. Thus neurogenic gene functions appear to be required both for the normal segregation of founder cells and for muscle differentiation. It is not clear whether either of these requirements reflects an essential function for any or all of the neurogenic genes within the mesoderm itself.
Cell polarity in early C. elegans development
Authors: Goldstein Bob , Hird Steven N. , White John G. 
Published: April 2021

ABSTRACT
The polarization of the embryonic axes is a key event in embryogenesis, being one of the earliest manifestations of the shape and form of the organism. The acquisition of polarity by individual blastomeres is one of the earliest indicators of commitment to a particular pathway of differentiation. These phenomena have been studied in the development of C. elegans both at the cellular and organismal level. This review summarizes what is known about how polarity is established in the blastomeres of this organism, how the division axes of polarized cells are determined, and how the embryonic axes are set up.
Investigations into the control of cell form and polarity: the use of morphological mutants in fission yeast
Authors: Snell Valery , Nurse Paul 
Published: April 2021

ABSTRACT
The fission yeast has been extensively used for investi-gating the cell cycle and is now being used to initiate studies into the control of cell form. There are a number of factors contributing to the generation of polarity in this organism, which are closely linked with the control of the cell cycle, including the redistributions of cytoskeletal components throughout the cycle and their correlation with patterns of end growth seen at different cell cycle stages. The controlled positioning of elements such as the nucleus and septum with respect to other cellular structures in order to produce viable daughter cells is clearly an important part of the fission yeast life cycle. This review will describe work already published concerning the control of cell form in this organism, including the isolation of various mutants displaying abnormal polarity, and will introduce work currently in progress to identify new elements involved in this control.
Digital malformations in the mouse foetus caused by X-radiation during pregnancy
Authors: Nogami Hiroshi 
Published: April 2021

ABSTRACT
Six groups of mice of the ddN-strain were exposed to a single, whole body X-radiation of 200 r. on the different days between the 8th and the 13th day of pregnancy. Others were exposed to 150 r. or 300 r. on the 12th day of pregnancy. Mice of the CF1strain were also exposed to 200 r. on the 12th day of pregnancy. Embryonic and foetal digits were examined both externally and microscopically 2, 6, 12, 18, 24, 48 and 72 hr. after X-radiation. After that they were examined at 1-day intervals until the 19th day of foetal age. Their ossified skeleton was studied by the Dawson method and their cartilaginous one was studied by Noback’s modification of van Wijhe’s method. The critical stage for digital malformations in the ddN-mouse was presumed to be in the beginning of the 12th day of embryonic stage. Digital rays with precartilage concentrations of the mesenchyme became obvious at this period. The incidence of digital malformations was proportional to the X-ray dose employed. Most malformations were of the reduction type, i.e. partial or complete ectrodactylism. The number of digits missing was proportional to the X-ray dose. The 2nd and the 3rd digits were most susceptible, while the 4th digit was most resistant. It was noticed that each malformation manifested itself also in various transitional forms. Differences between the ddN- and the CF1-strain in their tendency to manifest digital abnormalities were observed. Localized foci of cellular necrosis were already evident in the primordia of the digital bud 2 hr. after X-radiation and the pyknotic nuclei were almost eliminated after 24 hr. The prospective pattern of malformations could already be detected externally before the cleft between the digits became marked.