bluuebunny/crossref_metadata_2025_split huggingface dataset:
Developmental potency of the murine allantois
Authors: Downs Karen M. , Harmann Christine 
Published: April 2021

ABSTRACT
The murine allantois is the future umbilical component of the placenta. The base of the allantois is also thought to contain the future germ line. We have examined the fate and developmental potency of cells within the murine allantois during gastrulation.
lacZ-expressing headfold-stage allantoises (approximately 8.0 days postcoitum; dpc) were subdivided into three proximodistal regions and transplanted into three sites in synchronous non-transgenic host embryos: the primitive streak at the level of prospective paraxial mesoderm, the primitive streak at the level of lateral plate mesoderm, and the base of the allantois. After 23 hours in culture, operated conceptuses were examined histologically for contribution of donor allantoic cells to the conceptus. None of the allantoic regions contributed to paraxial mesoderm when placed into the fetus, but all three colonized the endothelium and adjacent mesenchyme of the dorsal aorta. The mid-region was most efficient at colonizing endothelium, whereas the base was the only allantoic region to exhibit relative pluripotency, colonizing several derivatives of all three primary germ layers.
Differences in the state of differentiation along the proximodistal axis of the allantois were further borne out when the three allantoic regions were placed into the base of the allantois of host conceptuses. Striking differences were observed in final position along the proximodistal axis of the host allantois. Most grafted cells translocated distally from the base; however, basal donor allantoic cells translocated typically only as far as the host’s mid-region, whereas donor allantoic tip cells typically returned to the tip, often colonizing the chorioallantoic fusion junction. Together, our data reveal that the headfold-stage allantois may contain a proximodistal gradient of differentiation, and raise intriguing questions about how this gradient was established and the role it plays in umbilical vasculogenesis.
A novel prespore-cell-inducing factor in Dictyostelium discoideum induces cell division of prespore cells
Authors: Oohata Akiko A. , Nakagawa Manabu , Tasaka Masao , Fujii Shigeru 
Published: April 2021

ABSTRACT
In Dictyostelium discoideum strain V12M2, at a very low cell density (∼102 cells/cm2), most amoebae differentiate into prespore cells in a salt solution containing cAMP if an adequately diluted conditioned medium (CM) is provided (Oohata, A. A. (1995)Differentiation 59, 283288). This finding suggests the presence of factor(s) released into the medium that are involved in inducing prespore cell differentiation. In the present study, we report the presence of two types of factors that function synergistically in prespore cell induction; one is a heatstable and dialysable factor(s) and the other is a heatlabile and non-dialysable factor termed psi (Ψ) factor (prespore-inducing factor). We purified and characterized the psi factor. Its relative molecular mass was determined to be 106×103Mr by SDS-PAGE and 180×103Mr by gel filtration HPLC, respectively. These results indicate that psi factor exists as a dimer under native conditions. In addition to inducing prespore cell differentiation, psi factor induced cell division of prespore cells in submerged culture. Our results suggest that psi factor plays important roles not only in prespore cell differentiation but also in the progress of the cell cycle in the prespore pathway in normal development.
Infection of the germ line by retroviral particles produced in the follicle cells: a possible mechanism for the mobilization of the gypsy retroelement of Drosophila
Authors: Song Sun U. , Kurkulos M. , Boeke Jef D. , Corces Victor G. 
Published: April 2021

ABSTRACT
The gypsy retroelement of Drosophila moves at high frequency in the germ line of the progeny of females carrying a mutation in the flamenco (flam) gene. This high rate of de novo insertion correlates with elevated accumulation of full-length gypsy RNA in the ovaries of these females, as well as the presence of an env-specific RNA. We have prepared monoclonal antibodies against the gypsy Pol and Env products and found that these proteins are expressed in the ovaries of flam females and processed in the manner characteristic of vertebrate retroviruses. The Pol proteins are expressed in both follicle and nurse cells, but they do not accumulate at detectable levels in the oocyte. The Env proteins are expressed exclusively in the follicle cells starting at stage 9 of oogenesis, where they accumulate in the secretory apparatus of the endoplasmic reticulum. They then migrate to the inner side of the cytoplasmic membrane where they assemble into viral particles. These particles can be observed in the perivitelline space starting at stage 10 by immunoelectron microscopy using anti-Env antibodies. We propose a model to explain flamenco-mediated induction of gypsy mobilization that involves the synthesis of gypsy viral particles in the follicle cells, from where they leave and infect the oocyte, thus explaining gypsy insertion into the germ line of the subsequent generation.
The bicoid-related homeoprotein Ptx1 defines the most anterior domain of the embryo and differentiates posterior from anterior lateral mesoderm
Authors: Lanctôt Christian , Lamolet Bruno , Drouin Jacques 
Published: April 2021

ABSTRACT
Ptx1 is a member of the small bicoid family of homeoboxcontaining genes; it was isolated as a tissue-restricted transcription factor of the pro-opiomelanocortin gene. Its expression during mouse and chick embryogenesis was determined by in situ hybridization in order to delineate its putative role in development. In the head, Ptx1 expression is first detected in the ectoderm-derived stomodeal epithelium at E8.0. Initially, expression is only present in the stomodeum and in a few cells of the rostroventral foregut endoderm. A day later, Ptx1 mRNA is detected in the epithelium and in a streak of mesenchyme of the first branchial arch, but not in other arches. Ptx1 expression is maintained in all derivatives of these structures, including the epithelia of the tongue, palate, teeth and olfactory system, and in Rathke’s pouch. Expression of Ptx1 in craniofacial structures is strikingly complementary to the pattern of goosecoid expression. In addition, Ptx1 is expressed early (E6.8) in posterior and extraembryonic mesoderm, and in structures that derive from these. The restriction of expression to the posterior lateral plate is later evidenced by exclusive labelling of the hindlimb but not forelimb mesenchyme. In the anterior domain of expression, the stomodeum was shown by fate mapping to derive from the anterior neural ridge (ANR) which represents the most anterior domain of the embryo. The concordance between these fate maps and the stomodeal pattern of Ptx1 expression supports the hypothesis that Ptx1 defines a stomodeal ectomere, which lies anteriorly to the neuromeres that have been suggested to constitute units of a segmented plan directing head formation.
Genetic basis of the formation and identity of type I and type II neurons in Drosophila embryos
Authors: Vervoort Michel , Merritt David J. , Ghysen Alain , Dambly-Chaudière Christine 
Published: April 2021

ABSTRACT
The embryonic peripheral nervous system of Drosophila contains two main types of sensory neurons: type I neurons, which innervate external sense organs and chordotonal organs, and type II multidendritic neurons. Here, we analyse the origin of the difference between type I and type II in the case of the neurons that depend on the proneural genes of the achaete-scute complex (ASC). We show that, in Notch− embryos, the type I neurons are missing while type II neurons are produced in excess, indicating that the type I/type II choice relies on Notch-mediated cell communication. In contrast, both type I and type II neurons are absent in numb− embryos and after ubiquitous expression of tramtrack, indicating that the activity of numb and the absence of tramtrack are required to produce both external sense organ and multidendritic neural fates. The analysis of string− embryos reveals that when the precursors are unable to divide they differentiate mostly into type II neurons, indicating that the type II is the default neuronal fate. We also report a new mutant phenotype where the ASC-dependent neurons are converted into type II neurons, providing evidence for the existence of one or more genes required for maintaining the alternative (type I) fate. Our results suggest that the same mechanism of type I/type II specification may operate at a late step of the ASCdependent lineages, when multidendritic neurons arise as siblings of the external sense organ neurons and, at an early step, when other multidendritic neurons precursors arise as siblings of external sense organ precursors.
First evidence of a calcium transient in flowering plants at fertilization
Authors: Digonnet C. , Aldon D. , Leduc N. , Dumas C. , Rougier M. 
Published: April 2021

ABSTRACT
We report here the first evidence of a transient elevation of free cytosolic Ca2+ following fusion of sperm and egg cell in a flowering plant by the use of an in vitro fertilization system recently developed in maize. Imaging changes in cytosolic Ca2+ at fertilization was undertaken by egg cell loading with the fluorescent Ca2+ indicator dye fluo-3 under controlled physiological conditions. The gamete adhesion step did not induce any cytosolic Ca2+ variation in the egg cell, whereas the fusion step triggered a transient cytosolic Ca2+ rise in the fertilized egg cell, lasting several minutes. This rise occurred after the establishment of gamete cytoplasm continuity. Through these observations, we open the way to the identification of the early signals induced by fertilization in flowering plants that give rise to the calcium transient and to investigations of the role of Ca2+ during egg activation and early zygote development in plants, as has been reported for other better character-ized animal and algae systems.
The role of lin-22, a hairy/Enhancer of split homolog, in patterning the peripheral nervous system of C. elegans
Authors: Wrischnik Lisa A. , Kenyon Cynthia J. 
Published: April 2021

ABSTRACT
In C. elegans, six lateral epidermal stem cells, the seam cells V1-V6, are located in a row along the anterior-posterior (A/P) body axis. Anterior seam cells (V1-V4) undergo a fairly simple sequence of stem cell divisions and generate only epidermal cells. Posterior seam cells (V5 and V6) undergo a more complicated sequence of cell divisions that include additional rounds of stem cell proliferation and the production of neural as well as epidermal cells. In the wild type, activity of the gene lin-22 allows V1-V4 to generate their normal epidermal lineages rather than V5-like lineages. lin-22 activity is also required to prevent additional neurons from being produced by one branch of the V5 lineage. We find that the lin-22 gene exhibits homology to the Drosophila gene hairy, and that lin-22 activity represses neural development within the V5 lineage by blocking expression of the posterior-specific Hox gene mab-5 in specific cells. In addition, in order to prevent anterior V cells from generating V5-like lineages, wild-type lin-22 gene activity must inhibit (directly or indirectly) at least five downstream regulatory gene activities. In anterior body regions, lin-22(+) inhibits expression of the Hox gene mab-5. It also inhibits the activity of the achaete-scute homolog lin-32 and an unidentified gene that we postulate regulates stem cell division. Each of these three genes is required for the expression of a different piece of the ectopic V5-like lineages generated in lin-22 mutants. In addition, lin-22 activity prevents two other Hox genes, lin-39 and egl-5, from acquiring new activities within their normal domains of function along the A/P body axis. Some, but not all, of the patterning activities of lin-22 in C. elegans resemble those of hairy in Drosophila.
An actin-mediated two-step mechanism is required for ventral enclosure of the C. elegans hypodermis
Authors: Williams-Masson Ellen M. , Malik Amy N. , Hardin Jeff 
Published: April 2021

ABSTRACT
The epiboly of the Caenorhabditis elegans hypodermis involves the bilateral spreading of a thin epithelial sheet from the dorsal side around the embryo to meet at the ventral midline in a process known as ventral enclosure. We present evidence that ventral enclosure occurs in two major steps. The initial migration of the hypodermis is led by a quartet of cells, which exhibit protrusive activity at their medial tips and are required to pull the hypodermis around the equator of the embryo. These cells display actin-rich filopodia and treatment with cytochalasin D immediately halts ventral enclosure, as does laser inactivation of all four cells. Once the quartet of cells has migrated around the equator of the embryo and approaches the ventral midline, the remainder of the leading edge becomes visible on the ventral surface and exhibits a localization of actin micro-filaments along the free edges of the cells, forming an actin ring. Cytochalasin D and laser inactivation block ventral enclosure at this later stage as well and, based upon phalloidin staining, we propose that the second half of enclosure is dependent upon a purse string mechanism, in which the actin ring contracts and pulls together the edges of the hypodermal sheet at the ventral midline. The ventral cells then form junctions with their contralateral neighbors to complete ventral enclosure.
Specification of the anterior hindbrain and establishment of a normal mid/hindbrain organizer is dependent on Gbx2 gene function
Authors: Wassarman Karen Montzka , Lewandoski Mark , Campbell Kenneth , Joyner Alexandra L. , Rubenstein John L. R. , Martinez Salvador , Martin Gail R. 
Published: April 2021

ABSTRACT
Analysis of mouse embryos homozygous for a loss-of-function allele of Gbx2 demonstrates that this homeobox gene is required for normal development of the mid/hindbrain region. Gbx2 function appears to be necessary at the neural plate stage for the correct specification and normal proliferation or survival of anterior hindbrain precursors. It is also required to maintain normal patterns of expression at the mid/hindbrain boundary of Fgf8 and Wnt1, genes that encode signaling molecules thought to be key components of the mid/hindbrain (isthmic) organizer. In the absence of Gbx2 function, isthmic nuclei, the cerebellum, motor nerve V, and other derivatives of rhombomeres 1-3 fail to form. Additionally, the posterior midbrain in the mutant embryos appears to be extended caudally and displays abnormalities in anterior/posterior patterning. The failure of anterior hindbrain development is presumably due to the loss of Gbx2 function in the precursors of the anterior hindbrain. However, since Gbx2 expression is not detected in the midbrain it seems likely that the defects in midbrain anterior/posterior patterning result from an abnormal isthmic signaling center. These data provide genetic evidence for a link between patterning of the anterior hindbrain and the establishment of the mid/hindbrain organizer, and identify Gbx2 as a gene required for these processes to occur normally.
The prechordal region lacks neural inducing ability, but can confer anterior character to more posterior neuroepithelium
Authors: Foley Ann C. , Storey Kate G. , Stern Claudio D. 
Published: April 2021

ABSTRACT
The avian equivalent of Spemann’s organizer, Hensen’s node, begins to lose its ability to induce a nervous system from area opaca epiblast cells at stage 4+, immediately after the full primitive streak stage. From this stage, the node is no longer able to induce regions of the nervous system anterior to the hindbrain. Stage 4+ is marked by the emergence from the node of a group of cells, the prechordal mesendoderm. Here we have investigated whether the prechordal region possesses the lost functions of the organizer, using quail-chick chimaeras to distinguish graft- and host-derived cells, together with several region-specific molecular markers. We find that the prechordal region does not have neural inducing ability, as it is unable to divert extraembryonic epiblast cells to a neural fate. However, it can confer more anterior character to prospective hindbrain cells of the host, making them acquire expression of the forebrain markers tailless and Otx-2. It can also rescue the expression of Krox-20 and Otx-2 from nervous system induced by an older (stage 5) node in extraembryonic epiblast. We show that these properties reflect a true change of fate of cells rather than recruitment from other regions. The competence of neuroectoderm to respond to anteriorizing signals declines by stages 7-9, but both posteriorizing signals and the ability of neuroectoderm to respond to them persist after this stage.
HSP70-2 is required for CDC2 kinase activity in meiosis I of mouse spermatocytes
Authors: Zhu Dahai , Dix David J. , Eddy E. M. 
Published: April 2021

ABSTRACT
Cyclin B-dependent CDC2 kinase activity has a key role in triggering the G2/M-phase transition during the mitotic and meiotic cell cycles. The Hsp70-2 gene is expressed only in spermatogenic cells at a significant level. In Hsp70-2 gene knock-out (Hsp70-2−/−) mice, primary spermatocytes fail to complete meiosis I, suggesting a link between HSP70-2 heat-shock protein and CDC2 kinase activity during this phase of spermatogenesis. Members of the HSP70 protein family are molecular chaperones that mediate protein de novo folding, translocation and multimer assembly. This study used immunoprecipitation-coupled western blot and in vitro reconstitution experiments to show that HSP70-2 interacts with CDC2 in the mouse testis, appears to be a molecular chaperone for CDC2, and is required for CDC2/cyclin B1 complex formation. Previous studies reported that most CDC2 kinase activity in the mouse testis is present in pachytene spermatocytes. Although CDC2 kinase activity for histone H1 was present in the testis of wild-type mice, it was nearly absent from the testis of Hsp70-2−/− mice, probably due to defective CDC2/cyclin B1 complex formation. Furthermore, addition of HSP70-2 to freshly prepared extracts of testis from Hsp70-2−/− mice not only restored CDC2/cyclin B1 complex formation but also reconstituted CDC2 kinase activity in vitro. It appears that one cause of failure to complete meiosis I during spermatogenesis in Hsp70-2−/− mice is disruption of CDC2/cyclin B1 assembly in pachytene spermatocytes, thereby preventing development of the CDC2 kinase activity required to trigger G2/M-phase transition. These studies provide novel in vivo evidence for a link between an HSP70 molecular chaperone and CDC2 kinase activity essential for the meiotic cell cycle in spermatogenesis.
Xenopus msx1 mediates epidermal induction and neural inhibition by BMP4
Authors: Suzuki Atsushi , Ueno Naoto , Hemmati-Brivanlou Ali 
Published: April 2021

ABSTRACT
Epidermal fate in Xenopus ectoderm has been shown to be induced by a secreted growth factor, Bone Morphogenetic Protein 4 (BMP4). However, the molecular mechanism mediating this response is poorly understood. Here, we show that the expression of the homeobox gene, msx1, is an immediate early response to BMP4 in Xenopus embryos. The timing of expression and embryonic distribution of msx1 parallel those described for BMP4. Moreover, over-expression of msx1 in early Xenopus embryos leads to their ventralization as described for BMP4. Consistent with mediating a BMP type of signaling, overexpression of msx1 is sufficient to induce epidermis in dissociated ectoderm cells, which would otherwise form neural tissue. Finally, msx1 can also rescue neuralization imposed by a dominant negative BMP receptor (tBR) in ectodermal explants. We propose that Xenopus msx1 acts as a mediator of BMP signaling in epidermal induction and inhibition of neural differentiation.
Mouse Dll3: a novel divergent Delta gene which may complement the function of other Delta homologues during early pattern formation in the mouse embryo
Authors: Dunwoodie Sally L. , Henrique Domingos , Harrison Stephen M. , Beddington Rosa S. P. 
Published: April 2021

ABSTRACT
Mouse delta-like 3 (Dll3), a novel vertebrate homologue of the Drosophila gene Delta was isolated by a subtracted library screen. In Drosphila, the Delta/Notch signalling pathway functions in many situations in both embryonic and adult life where cell fate specification occurs. In addition, a patterning role has been described in the establishment of the dorsoventral compartment boundary in the wing imaginal disc. Dll3 is the most divergent Delta homologue identified to date. We confirm that Dll3 can inhibit primary neurogenesis when ectopically expressed in Xenopus, suggesting that it can activate the Notch receptor and therefore is a functional Delta homologue. An extensive expression study during gastrulation and early organogenesis in the mouse reveals a diverse and dynamic pattern of expression. The three major sites of expression implicate Dll3 in somitogenesis and neurogenesis and in the production of tissue from the primitive streak and tailbud. A careful comparison of Dll3 and Dll1 expression by double RNA in situ hybridisation demonstrates that these genes have distinct patterns of expression, but implies that together they operate in many of the same processes. We postulate that during somitogenesis Dll3 and Dll1 coordinate in establishing the intersomitic boundaries. We confirm that, during neurogenesis in the spinal cord, Dll1 and Dll3 are expressed by postmitotic cells and suggest that expression is sequential such that cells express Dll1 first followed by Dll3. We hypothesise that Dll1 is involved in the release of cells from the precursor population and that Dll3 is required later to divert neurons along a specific differentiation pathway.
Genetically engineered mice demonstrate that adenosine deaminase is essential for early postimplantation development
Authors: Blackburn Michael R. , Knudsen Thomas B. , Kellems Rodney E. 
Published: April 2021

ABSTRACT
Adenosine deaminase (ADA) is an essential enzyme of purine metabolism that is enriched at the maternal-fetal interface of mice throughout postimplantation development. During early postimplantation stages Ada is highly expressed in both maternally derived decidual cells and zygotically derived trophoblast cells. For the current study we utilized genetically modified mice to delineate the relative contribution and importance of decidual and trophoblast ADA at the maternal-fetal interface. In females genetically engineered to lack decidual ADA a striking pattern of expression was revealed in giant trophoblast cells that surround the early postimplantation embryo. Embryos within gestation sites lacking both decidual and trophoblast ADA died during the early postimplantation period, whereas expression in trophoblast cells alone was sufficient for survival through this period. Severe disturbances in purine metabolism were observed in gestation sites lacking decidual ADA, including the accumulation of the potentially toxic ADA substrates adenosine and 2′-deoxyadenosine. These experiments provide genetic evidence that Ada expression at the maternal-fetal interface is essential for early postimplantation development in mice.