bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of the growth/differentiation transition in Dictyostelium development by transient expression of a novel gene, dia1
Authors: Hirose Shigenori , Inazu Yuji , Chae Soo-Cheon , Maeda Yasuo 
Published: April 2021

ABSTRACT
In Dictyostelium discoideum Ax-2 cells, a specific checkpoint (PS point) from which cells enter the differentiation phase in response to starvation has been specified in the cell cycle. Using the differential display method, we isolated a novel gene, dia1 (differentiation-associated gene 1), that is specifically expressed in cells differentiating from the PS point. The dia1 mRNA has an open reading frame of 1,368 bp and is deduced to code for a 48.6 kDa protein (DIA1). The DIA1 protein is highly serine-rich and the serine residues are predominantly located in the C-terminal region. After the PSORT II search, the protein is predicted to be GPI-anchored at the plasma membrane. Unexpectedly, dia1 overexpression rather impaired the progression of differentiation, possibly coupled with the reduced expression of early genes such as cAMP receptor1 (car1). The inhibitory effect of dia1 expression on early differentiation was almost completely nullified by externally applied cAMP pulses. In contrast to dia1 overexpression, antisense RNA-mediated dia1 inactivation was found to enhance the initial step of cell differentiation, as exemplified by precocious expression of car1 and other early genes. We discuss the unique structure and function of DIA1 in relation to the cooperative development of cells during the establishment of multicellular organization.
TORNADO1 and TORNADO2 are required for the specification of radial and circumferential pattern in the Arabidopsis root
Authors: Cnops Gerda , Wang Xuan , Linstead Paul , Montagu Marc Van , Lijsebettens Mieke Van , Dolan Liam 
Published: April 2021

ABSTRACT
The cell layers of the Arabidopsis primary root are arranged in a simple radial pattern. The outermost layer is the lateral root cap and lies outside the epidermis that surrounds the ground tissue. The files of epidermal and lateral root cap cells converge on a ring of initials (lateral root cap/epidermis initial) from which the epidermal and lateral root cap tissues of the seedling are derived, once root growth is initiated after germination. Each initial gives rise to a clone of epidermal cells and a clone of lateral root cap cells. These initial divisions in the epidermal/lateral root cap initial are defective in tornado1 (trn1) and trn2 plants indicating a requirement for TRN1 and TRN2 for initial cell function. Furthermore, lateral root cap cells develop in the epidermal position in trn1 and trn2 roots indicating that TRN1 and TRN2 are required for the maintenance of the radial pattern of cell specification in the root. The death of these ectopic lateral root cap cells in the elongation zone (where lateral root cap cells normally die) results in the development of gaps in the epidermis. These observations indicate that TRN1 and TRN2 are required to maintain the distinction between the lateral root cap and epidermis and suggest that lateral root cap fate is the default state. It also suggests that TRN1 and TRN2 repress lateral root cap fate in cells in the epidermal location. Furthermore, the position-dependent pattern of root hair and non-root hair cell differentiation in the epidermis is defective in trn1 and trn2 mutants. Together these results indicate that TRN1 and TRN2 are required for the maintenance of both the radial pattern of tissue differentiation in the root and for the subsequent circumferential pattern within the epidermis.
Animal and vegetal poles of the mouse egg predict the polarity of the embryonic axis, yet are nonessential for development
Authors: Ciemerych Maria Anna , Mesnard Daniel , Zernicka-Goetz Magdalena 
Published: April 2021

ABSTRACTRecent studies suggest early (preimplantation) events might be important in the development of polarity in mammalian embryos. We report here lineage tracing experiments with green fluorescent protein showing that cells located either near to or opposite the polar body at the 8-cell stage of the mouse embryo retain their same relative positions in the blastocyst. Thus they come to lie on either end of an axis of symmetry of the blastocyst that has recently been shown to correlate with the anterior-posterior axis of the postimplantation embryo (see R. J. Weber, R. A. Pedersen, F. Wianny, M. J. Evans and M. Zernicka-Goetz (1999). Development 126, 5591-5598). The embryonic axes of the mouse can therefore be related to the position of the polar body at the 8-cell stage, and by implication, to the animal-vegetal axis of the zygote. However, we also show that chimeric embryos constructed from 2-cell stage blastomeres from which the animal or the vegetal poles have been removed can develop into normal blastocysts and become fertile adult mice. This is also true of chimeras composed of animal or vegetal pole cells derived through normal cleavage to the 8-cell stage. We discuss that although polarity of the postimplantation embryo can be traced back to the 8-cell stage and in turn to the organisation of the egg, it is not absolutely fixed by this time.
In vivo induction of cardiac Purkinje fiber differentiation by coexpression of preproendothelin-1 and endothelin converting enzyme-1
Authors: Takebayashi-Suzuki Kimiko , Yanagisawa Masashi , Gourdie Robert G. , Kanzawa Nobuyuki , Mikawa Takashi 
Published: April 2021

ABSTRACT
The rhythmic heart beat is coordinated by electrical impulses transmitted from Purkinje fibers of the cardiac conduction system. During embryogenesis, the impulse-conducting cells differentiate from cardiac myocytes in direct association with the developing endocardium and coronary arteries, but not with the venous system. This conversion of myocytes into Purkinje fibers requires a paracrine interaction with blood vessels in vivo, and can be induced in vitro by exposing embryonic myocytes to endothelin-1 (ET-1), an endothelial cell-associated paracrine factor. These results suggest that an endothelial cell-derived signal is capable of inducing juxtaposed myocytes to differentiate into Purkinje fibers. It remains unexplained how Purkinje fiber recruitment is restricted to subendocardial and periarterial sites but not those juxtaposed to veins. Here we show that while the ET-receptor is expressed throughout the embryonic myocardium, introduction of the ET-1 precursor (preproET-1) in the embryonic myocardium is not sufficient to induce myocytes to differentiate into conducting cells. ET converting enzyme-1 (ECE-1), however, is expressed preferentially in endothelial cells of the endocardium and coronary arteries where Purkinje fiber recruitment takes place. Retroviral-mediated coexpression of both preproET-1 and ECE-1 in the embryonic myocardium induces myocytes to express Purkinje fiber markers ectopically and precociously. These results suggest that expression of ECE-1 plays a key role in defining an active site of ET signaling in the heart, thereby determining the timing and location of Purkinje fiber differentiation within the embryonic myocardium.
Ecdysteroid coordinates optic lobe neurogenesis via a nitric oxide signaling pathway
Authors: Champlin David T. , Truman James W. 
Published: April 2021

ABSTRACT
Proliferation of neural precursors in the optic lobe of Manduca sexta is controlled by circulating steroids and by local production of nitric oxide (NO). Diaphorase staining, anti-NO synthase (NOS) immunocytochemistry and the NO-indicator, DAF-2, show that cells throughout the optic anlage contain NOS and produce NO. Signaling via NO inhibits proliferation in the anlage. When exposed to low levels of ecdysteroid, NO production is stimulated and proliferation ceases. When steroid levels are increased, NO production begins to decrease within 15 minutes independent of RNA or protein synthesis and cells rapidly resume proliferation. Resumption of proliferation is not due simply to the removal of NO repression though, but also requires an ecdysteroid stimulatory pathway. The consequence of these opposing pathways is a sharpening of the responsiveness to the steroid, thereby facilitating a tight coordination between development of the different elements of the adult visual system.
Two different activities ofSuppressor of Hairlessduring wing development inDrosophila
Authors: Klein Thomas , Seugnet Laurent , Haenlin Marc , Arias Alfonso Martinez 
Published: April 2021

ABSTRACTThe Notch pathway plays a crucial and universal role in the assignation of cell fates during development. In Drosophila, Notch is a transmembrane protein that acts as a receptor of two ligands Serrate and Delta. The current model of Notch signal transduction proposes that Notch is activated upon binding its ligands and that this leads to the cleavage and release of its intracellular domain (also called Nintra). Nintra translocates to the nucleus where it forms a dimeric transcription activator with the Su(H) protein. In contrast with this activation model, experiments with the vertebrate homologue of Su(H), CBF1, suggest that, in vertebrates, Nintra converts CBF1 from a repressor into an activator. Here we have assessed the role of Su(H) in Notch signalling during the development of the wing of Drosophila. Our results show that, during this process, Su(H) can activate the expression of some Notch target genes and that it can do so without the activation of the Notch pathway or the presence of Nintra. In contrast, the activation of other Notch target genes requires both Su(H) and Nintra, and, in the absence of Nintra, Su(H) acts as a repressor. We also find that the Hairless protein interacts with Notch signalling during wing development and inhibits the activity of Su(H). Our results suggest that, in Drosophila, the activation of Su(H) by Notch involve the release of Su(H) from an inhibitory complex, which contains the Hairless protein. After its release Su(H) can activate gene expression in absence of Nintra.
sog and dpp exert opposing maternal functions to modify Toll signaling and pattern the dorsoventral axis of the Drosophila embryo
Authors: Araujo H. , Bier E. 
Published: April 2021

ABSTRACT
The short gastrulation (sog) and decapentaplegic (dpp) genes function antagonistically in the early Drosophila zygote to pattern the dorsoventral (DV) axis of the embryo. This interplay between sog and dpp determines the extent of the neuroectoderm and subdivides the dorsal ectoderm into two territories. Here, we present evidence that sog and dpp also play opposing roles during oogenesis in patterning the DV axis of the embryo. We show that maternally produced Dpp increases levels of the IkB-related protein Cactus and reduces the magnitude of the nuclear concentration gradient of the NFkB-related Dorsal protein, and that Sog limits this effect. We present evidence suggesting that Dpp signaling increases Cactus levels by reducing a signal-independent component of Cactus degradation. Epistasis experiments reveal that sog and dpp act downstream of, or in parallel to, the Toll receptor to reduce translocation of Dorsal protein into the nucleus. These results broaden the role previously defined for sog and dpp in establishing the embryonic DV axis and reveal a novel form of crossregulation between the NFkB and TGFβ signaling pathways in pattern formation.
The olfactory placodes of the zebrafish form by convergence of cellular fields at the edge of the neural plate
Authors: Whitlock Kathleen E. , Westerfield Monte 
Published: April 2021

ABSTRACTThe primary olfactory sensory system is part of the PNS that develops from ectodermal placodes. Several cell types, including sensory neurons and support cells, differentiate within the olfactory placode to form the mature olfactory organ. The olfactory placodes are thought to arise from lateral regions of the anterior neural plate, which separate from the plate through differential cell movements. We determined the origins of the olfactory placodes in zebrafish by labeling cells along the anterior-lateral edge of the neural plate at times preceding the formation of the olfactory placodes and examining the later fates of the labeled cells. Surprisingly, we found that the olfactory placode arises from a field of cells, not from a discrete region of the anterior neural plate. This field extends posteriorly to the anterior limits of cranial neural crest and is bordered medially by telencephalic precursors. Cells giving rise to progeny in both the olfactory organ and telencephalon express the distal-less 3 gene. Furthermore, we found no localized pockets of cell division in the anterior-lateral neural plate cells preceding the appearance of the olfactory placode. We suggest that the olfactory placodes arise by anterior convergence of a field of lateral neural plate cells, rather than by localized separation and proliferation of a discrete group of cells.
Some fly sensory organs are gliogenic and require glide/gcm in a precursor that divides symmetrically and produces glial cells
Authors: Van De Bor Veronique , Walther Rachel , Giangrande Angela 
Published: April 2021

ABSTRACT
In flies, the choice between neuronal and glial fates depends on the asymmetric division of multipotent precursors, the neuroglioblast of the central nervous system and the IIb precursor of the sensory organ lineage. In the central nervous system, the choice between the two fates requires asymmetric distribution of the glial cell deficient/glial cell missing (glide/gcm) RNA in the neuroglioblast. Preferential accumulation of the transcript in one of the daughter cells results in the activation of the glial fate in that cell, which becomes a glial precursor. Here we show that glide/gcm is necessary to induce glial differentiation in the peripheral nervous system. We also present evidence that glide/gcm RNA is not necessary to induce the fate choice in the peripheral multipotent precursor. Indeed, glide/gcm RNA and protein are first detected in one daughter of IIb but not in IIb itself. Thus, glide/gcm is required in both central and peripheral glial cells, but its regulation is context dependent. Strikingly, we have found that only subsets of sensory organs are gliogenic and express glide/gcm. The ability to produce glial cells depends on fixed, lineage related, cues and not on stochastic decisions. Finally, we show that after glide/gcm expression has ceased, the IIb daughter migrates and divides symmetrically to produce several mature glial cells. Thus, the glide/gcm-expressing cell, also called the fifth cell of the sensory organ, is indeed a glial precursor. This is the first reported case of symmetric division in the sensory organ lineage. These data indicate that the organization of the fly peripheral nervous system is more complex than previously thought.
The expression of Myf5 in the developing mouse embryo is controlled by discrete and dispersed enhancers specific for particular populations of skeletal muscle precursors
Authors: Summerbell Dennis , Ashby Peter R. , Coutelle Oliver , Cox David , Yee Siu-Pok , Rigby Peter W. J. 
Published: April 2021

ABSTRACT
The development of skeletal muscle in vertebrate embryos is controlled by a transcriptional cascade that includes the four myogenic regulatory factors Myf5, Myogenin, MRF4 and MyoD. In the mouse embryo, Myf5 is the first of these factors to be expressed and mutational analyses suggest that this protein acts early in the process of commitment to the skeletal muscle fate. We have therefore analysed the regulation of Myf5 gene expression using transgenic technology and find that its control is markedly different from that of the other two myogenic regulatory factor genes previously analysed, Myogenin and MyoD. We show that Myf5 is regulated through a number of distinct and discrete enhancers, dispersed throughout 14 kb spanning the MRF4/Myf5 locus, each of which drives reporter gene expression in a particular subset of skeletal muscle precursors. This region includes four separate enhancers controlling expression in the epaxial muscle precursors of the body, some hypaxial precursors of the body, some facial muscles and the central nervous system. These elements separately or together are unable to drive expression in the cells that migrate to the limb buds and in some other muscle subsets and to correctly maintain expression at late times. We suggest that this complex mechanism of control has evolved because different inductive signals operate in each population of muscle precursors and thus distinct enhancers, and cognate transcription factors, are required to interpret them.
TheArabidopsis COMATOSElocus regulates germination potential
Authors: Russell Laurel , Larner Victoria , Kurup Smita , Bougourd Susan , Holdsworth Michael 
Published: April 2021

ABSTRACTMutation of the COMATOSE locus in Arabidopsis results in a marked reduction in germination potential. Whilst the morphology of comatose (cts) embryos is not altered, physiological analysis reveals that mature cts seeds do not respond to gibberellin. Prolonged chilling of imbibed seeds only partially restores germination potential, and seeds do not after ripen. Genetic analysis shows that the cts phenotype is expressed in the embryo and phenotypic differences between wild-type and mutant plants were not observed during other stages of plant growth and development. Therefore cts represents a new class of mutant, with a specific lesion that results in severely impaired germination potential. Genetic interactions were analysed between cts and loci that regulate embryo maturation, and abscisic acid biosynthesis and perception. Results from these studies showed that the cts mutant phenotype required the wild-type action of these loci, and suggested that CTS exerts a repressive function on these loci.A model is presented postulating that CTS promotes increased germination potential, and represses embryo dormancy. These functions of CTS may result in the removal of embryo dormancy as a prerequisite to germination.
Serrate and Notch specify cell fates in the heart field by suppressing cardiomyogenesis
Authors: Rones Melissa S. , McLaughlin Kelly A. , Raffin Michael , Mercola Mark 
Published: April 2021

ABSTRACT
Notch signaling mediates numerous developmental cell fate decisions in organisms ranging from flies to humans, resulting in the generation of multiple cell types from equipotential precursors. In this paper, we present evidence that activation of Notch by its ligand Serrate apportions myogenic and non-myogenic cell fates within the early Xenopus heart field. The crescent-shaped field of heart mesoderm is specified initially as cardiomyogenic. While the ventral region of the field forms the myocardial tube, the dorsolateral portions lose myogenic potency and form the dorsal mesocardium and pericardial roof (Raffin, M., Leong, L. M., Rones, M. S., Sparrow, D., Mohun, T. and Mercola, M. (2000) Dev. Biol., 218, 326-340). The local interactions that establish or maintain the distinct myocardial and non-myocardial domains have never been described. Here we show that Xenopus Notch1 (Xotch) and Serrate1 are expressed in overlapping patterns in the early heart field. Conditional activation or inhibition of the Notch pathway with inducible dominant negative or active forms of the RBP-J/Suppressor of Hairless [Su(H)] transcription factor indicated that activation of Notch feeds back on Serrate1 gene expression to localize transcripts more dorsolaterally than those of Notch1, with overlap in the region of the developing mesocardium. Moreover, Notch pathway activation decreased myocardial gene expression and increased expression of a marker of the mesocardium and pericardial roof, whereas inhibition of Notch signaling had the opposite effect. Activation or inhibition of Notch also regulated contribution of individual cells to the myocardium. Importantly, expression of Nkx2.5 and Gata4 remained largely unaffected, indicating that Notch signaling functions downstream of heart field specification. We conclude that Notch signaling through Su(H) suppresses cardiomyogenesis and that this activity is essential for the correct specification of myocardial and non-myocardial cell fates.
Embryonic development is disrupted by modest increases in vascular endothelial growth factor gene expression
Authors: Miquerol Lucile , Langille B. Lowell , Nagy Andras 
Published: April 2021

ABSTRACT
Previous work has shown that heterozygocity for a null mutation of the VEGF-A gene, resulting in a 50% reduction in VEGF-A expression, is embryonic lethal at embroyonic day (E) 9.5 in mice. We now show that two-to threefold overexpression of VEGF-A from its endogenous locus results in severe abnormalities in heart development and embryonic lethality at E12.5-E14. The mutant embryos displayed an attenuated compact layer of myocardium, overproduction of trabeculae, defective ventricular septation and abnormalities in remodeling of the outflow track of the heart. In addition, aberrant coronary development was characterized by formation of oversized epicardial vessels, apparently through vasculogenesis. We infer that embryonic survival requires a narrow window of VEGF-A expression.
The Drosophila disembodied gene controls late embryonic morphogenesis and codes for a cytochrome P450 enzyme that regulates embryonic ecdysone levels
Authors: Chávez V. Marcela , Marqués Guillermo , Delbecque Jean Paul , Kobayashi Kayta , Hollingsworth Margarita , Burr John , Natzle Jeanette E. , O’Connor Michael B. 
Published: April 2021

ABSTRACT
Ecdysteroids regulate a wide variety of cellular processes during arthropod development, yet little is known about the genes involved in the biosynthesis of these hormones. Previous studies have suggested that production of 20-hydroxyecdysone in Drosophila and other arthropods involves a series of cytochrome P450 catalyzed hydroxylations of cholesterol. In this report, we show that the disembodied (dib) locus of Drosophila codes for a P450-like sequence. In addition, we find that dib mutant embryos have very low titers of ecdysone and 20-hydroxyecdysone (20E) and fail to express IMP-E1 and L1, two 20E-inducible genes, in certain tissues of the embryo. In situ hybridization studies reveal that dib is expressed in a complex pattern in the early embryo, which eventually gives way to restricted expression in the prothoracic portion of the ring gland. In larval and adult tissues, dib expression is observed in the prothoracic gland and follicle cells of the ovaries respectively, two tissues known to synthesize ecdysteroids. Phenotypic analysis reveals that dib mutant embryos produce little or no cuticle and exhibit severe defects in many late morphogenetic processes such as head involution, dorsal closure and gut development. In addition, we examined the phenotypes of several other mutants that produce defective embryonic cuticles. Like dib, mutations in the spook (spo) locus result in low embryonic ecdysteroid titers, severe late embryonic morphological defects, and a failure to induce IMP-E1. From these data, we conclude that dib and spo likely code for essential components in the ecdysone biosynthetic pathway and that ecdysteroids regulate many late embryonic morphogenetic processes such as cell movement and cuticle deposition.