WBbt:0004017 vs WBls:0000092

Application of Hg2+ (0.1-1 microM) had no effect on the basal [Ca2+]i of freshly dissociated cells (10th day in ovo) and cells in culture (the 4-day cultures from the telencephalon of 5-day-old embryos), but potentiated KA-induced increase of [Ca2+]i in a Ca-free-EGTA solution in a concentration-dependent manner.

While IL-3 does not appear to be required for mast cell development, these precursors do require the presence of a connective tissue microenvironment such as embryonic skin.

We identify 94 ncRNAs that have never been reported to regulate gene expressions, are co-expressed with 1208 protein-coding genes in cell type specific and/or embryo time specific manners.

I(Cl,mec) is not detectable in whole-cell or isolated patch recordings from oocytes, cultured muscle cells, and cultured neurons but is expressed in single cell and later embryos.

Evidence from genetically engineered mice does not support the view that insulin and IGF receptors promote cellular differentiation in vivo or that they are required for early embryonic development.

However, esterase does not appear in cytochalasin D blocked one-cell embryos.

Taken together, our results indicated that carbendazim had the potential to induce cell apoptosis and cause immune toxicity as well as endocrine disruption in zebrafish during the embryo developmental stage.

Experimentally induced depolarization of resting membrane potential in "instructor cells" in Xenopus laevis embryos causes hyperpigmentation in an all-or-none fashion in some tadpoles due to excess proliferation and migration of melanocytes.

In this study, we identified that oxidative stress responsive 1b (osr1b) is upregulated in endothelial cells in both embryonic and tumor-induced angiogenesis in zebrafish, accompanied by downregulation of protein phosphatase 2A (pp2a) subunit ppp2r1bb.

CMs were derived from human pluripotent stem cells (hPSCs), including human embryonic stem cells and induced pluripotent stem cells, using 2D and 3D differentiation methods.

The effects of suramin, an inhibitor of growth factor mitogenic activity, were evaluated on basic fibroblast growth factor (bFGF)-induced proliferation of bovine aortic endothelial cells and on angiogenesis in the chorioallantoic membrane (CAM) of chick embryos.

Whole-cell, voltage-clamp recordings from a human embryonic kidney cell line (HEK 293) stably expressing hGluR4 confirmed the presence of constitutively active, ligand-gated ion channels activated by AMPA, glutamate and kainate but not N-methyl-D-aspartate.

In addition, NF1 cells responded to dexamethasone by increasing the beta GP-induced mineralization, as opposed to cells from other embryonic bones, which either did not respond or have even decreased mineralization under dexamethasone.

We used clone 6 cells (rat embryo fibroblasts transformed by the temperature sensitive mutant p53val135 and an activated H-ras-gene (Michalovitz et al., 1990)), growth arrested at 32 degrees C, as a model to analyse whether and how transformed cells, growth-arrested by an overexpressed wild-type p53, might overcome p53-mediated growth inhibition.

Further studies showed that TRH (1-100 microM) and RGH-2202 (100 microM) significantly attenuated the kainate (150 microM)-induced lactate dehydrogenase release in a primary cortical cell culture from rat embryos.

Glucocorticoid (GC) plays a key role in controlling numerous cellular processes during embryogenesis and fetal development.

Prior attempts at beta cell regeneration have relied upon pancreatic injury to induce beta cell proliferation, dedifferentiation and activation of the embryonic pathway, or stem cell replacement.

Induced pluripotent stem cells (iPSCs) avoid many of the restrictions that hamper the application of human embryonic stem cells: limited availability of source material due to legal restrictions in some countries, immunogenic rejection and ethical concerns.

Independent of its low metabolic activity, proinsulin stimulates proliferation in developing neuroretina, as well as cell survival and cardiogenesis in early embryos.

However, cancer cells can be suppressed by young and quickly proliferating non-cancer cells, such as embryonic stem cells.

Lymphoid and bone marrow cells from normal and horse serum-immunized mice and lymphoid cells from Nippostrongylus brasiliensis-infected mice were cultured on monolayers of embryonic skin fibroblasts to analyze the factors which regulate the differentiation and proliferation of mast cells in vitro.

We have characterized the notochord malformation using histological and in situ hybridization techniques. collagen 2a1 mRNA expression is normally localized to the notochord sheath cells at 24 hpf, whereas in NaM-exposed embryos it is misexpressed in the notochord cells.

The members of the transforming growth factor β (TGF-β) family of cell signaling polypeptides have garnered a great deal of interest due to its capacity from nematodes to mammals to regulate cell-based activities which control the growth of embryos and sustain tissue homeostasis.

Then the effect of mmu-miR-92a-2-5p on S. japonicum-induced liver fibrosis including cell apoptosis rates, proliferation and proteins related to liver fibrosis was examined in NIH-3T3 mouse embryonic fibroblasts.

Members of the transforming growth factor beta (TGF-beta) superfamily of cell signalling polypeptides have attracted much attention because of their ability, from nematodes to mammals, to control cellular functions that in turn, regulate embryo development and tissue homeostasis.

Here we show that the MIF protein from B. glabrata (BgMIF) is expressed in circulating immune defense cells (hemocytes) of the snail as well as in the B. glabrata embryonic (Bge) cell line that has hemocyte-like features.

Members of the transforming growth factor beta superfamily of cell signaling polypeptides have attracted much attention because of their ability, from nematodes to mammals, to control cellular functions that in turn, regulate embryo development and tissue homeostasis (the transforming growth factors betas 95 (1990) 419).

Cell-cell interactions are thought to regulate the differential specification of secondary mesenchyme cells (SMCs) and endoderm in the sea urchin embryo.

In this study, we conducted comprehensive investigations utilizing human colorectal cancer HCT116 cells, human umbilical cord vascular endothelial cells (HUVECs), and zebrafish embryos to assess the potential benefits of DMA in suppressing tumor angiogenesis.

Human pluripotent stem cells (hPSCs; both embryonic and induced pluripotent) rapidly proliferate in adherent culture to maintain their undifferentiated state.

We show that the BbC functions as a cell-cell adhesion molecule when expressed in Drosophila S2 cells and localizes to adherens junctions in the ectodermal epithelia in amphioxus embryos.

Wnt proteins are a family of highly conserved secreted glycoproteins that regulate cell-to-cell interactions during embryogenesis.

The cell biology of intermediate filament (IF) proteins and their filaments is complicated by the fact that the members of the gene family, which in humans amount to at least 65, are differentially expressed in very complex patterns during embryonic development.

Here we report that nonchordate deuterostome Brachyury genes can trigger the differentiation of extra notochord cells when these genes are ectopically expressed in ascidian embryos.

The senseless (sens) gene is required for proper development of most cell types of the embryonic and adult peripheral nervous system (PNS) of Drosophila.

In Drosophila, ectopic Caudal in anterior cells can induce head defects, and in Caenorhabditis the absence of Caudal in anterior embryonic cells is required for proper development.

Dmnk mRNAs are transcribed in nurse cells and are subsequently localized in the anterior of oocytes during oogenesis, in a manner similar to several maternal transcripts regulating oogenesis and early embryogenesis.

The general requirement to induce mesoderm and allocate cells into different mesodermal tissues such as body muscle or heart is common in many animal embryos.

In most cells, chromosome segregation error is averted by the spindle assembly checkpoint (SAC), which prevents anaphase-promoting complex (APC/C) activation and anaphase onset until chromosomes are aligned with kinetochores attached to spindle microtubules [6, 7], but little is known about the SAC's role in the early mammalian embryo.

We demonstrate that ACRC/GCNA family SprT proteases interact with SUMO and establish important physiological roles of Caenorhabditis elegans GCNA-1 and SUMOylation in promoting germ cell and embryonic survival upon DPC formation.

Cell division timing is critical for cell fate specification and morphogenesis during embryogenesis, but how division timings are regulated among cells during development is poorly understood.

In this chapter, we review the basis for natural and induced cellular plasticity in C. elegans We describe the events that progressively restrict cellular differentiation during embryogenesis, starting with the multipotency-to-commitment transition (MCT) and subsequently through postembryonic development of the animal, and consider the range of molecular processes, including transcriptional and translational control systems, that contribute to cellular plasticity.

To validate this approach, we observe the radiation-induced damage, such as reduced cell mobility, incomplete cell division and the appearance of chromatin bridges during embryo development, in different strains expressing GFP-tagged proteins in situ after irradiation.

The current study provides strong evidence to support the notion that enhanced lipid peroxidation in G6PD deficiency promotes death of germ cells and impairs embryogenesis in C. elegans.

This asymmetric patterning is required for a number of biological processes including asymmetric division, cell migration, and embryonic development.

Beginning at the four-cell stage, and continuing throughout embryogenesis and larval development, mother cells are polarized by Wnt ligands, causing an asymmetric inheritance of key members of a Wnt/β-catenin signal transduction pathway termed the Wnt/β-catenin asymmetry pathway.

The heterochronic pathway in C. elegans controls the relative timing of cell fate decisions during post-embryonic development.

We find that the tension exerted on HMP-1 has a cell-specific distribution, is actomyosin-dependent, but is regulated differently from the tension on the actin cortex during embryonic elongation.

Here, we show that intron-derived miRNA is not only able to induce RNAi in mammalian cells but also in fish, chicken embryos, and adult mice cells, demonstrating the evolutionary preservation of this gene regulation system in vivo.

The PAR-1 kinase of C. elegans is localized to the posterior of the one-cell embryo and its mutations affect asymmetric spindle placement and partitioning of cytoplasmic components in the first cell cycle.

Many vital processes during C. elegans development, especially the establishment and maintenance of cell polarity in embryogenesis, are controlled by complex signaling pathways.

Previous high throughput cellular resolution expression studies identified dozens of transcription factors with lineage-specific expression patterns in C. elegans embryos that could regulate progenitor identity.

Our studies of epidermal cell migrations in developing Caenorhabditiselegans embryos have identified multiple plasma membrane signals that regulate the Rac GTPase, thus regulating WAVE and Arp2/3 complexes, to promote branched F-actin formation and polarized enrichment.

In Caenorhabditis elegans one-cell embryos, myosin localizes at the anterior cortex whereas the mitotic spindle localizes toward the posterior.

Here we discuss our current understanding and open questions on the mechanism by which the PAR proteins regulate asynchronous cell divisions in the early C. elegans embryo.

It functions as a guanine nucleotide exchange factor for Gαi, Gαq, and Gα12/13 and as a molecular chaperone required for the initial association of nascent Gα subunits with cellular membranes in embryonic stem cell lines.

In this issue of Developmental Cell, Elewa et al. (2015) show that combinatorial action of RNA binding proteins modulates poly(A) tail length of maternal mRNAs, leading to asymmetric expression of a cell fate determinant in early C. elegans embryos.

In the present paper, we describe how polarity cues, cytoskeleton and cell-to-cell communication interact with each other to regulate orientation of the early embryonic division planes in model animals such as Caenorhabditis elegans, Drosophila and mouse.

Like in lower species, 16S mtrRNA is found to localize in the cytoplasm outside of mitochondria in mouse 2-cell embryos.

To explore the mechanisms that determine checkpoint strength in different cells, we systematically measured the mitotic delay induced by microtubule disruption at different stages of embryogenesis in Caenorhabditis elegans.

We found that the DCC starts repressing the X chromosomes by the 40-cell stage, but X-linked transcript levels remain significantly higher in hermaphrodites compared to males through the comma stage of embryogenesis.

As is the case in most eukaryotic cell types, the replication stress response is controlled by the ATR kinase in early worm embryos.

To better understand how the cellular response to DNA replication stress is regulated during embryonic development, we and others have established the early C. elegans embryo as a model system to study this important problem.

The nucleosome remodeling and deacetylase complex promotes cell fate decisions throughout embryonic development.

Compression changes the relative positions of many cells and causes severe distortions of the embryonic axes.

Wnt proteins are best known for their profound roles in cell patterning, because they are required for the embryonic development of all animal species studied to date.

In the March 15, 2012, issue of Genes & Development, Kniazeva and colleagues (pp. 554-566) describe how the particular combination of a branched chain fatty acid and an acyl-CoA synthetase is required for critical cellular processes during early embryogenesis in Caenorhabditis elegans.

TOP-1β is broadly localized to the nuclei of many cells at all developmental stages and concentrated in nucleoli in embryo gut and oogenic cells.

We further determine that zTATDN1 is predominantly expressed in eye cells during embryonic development.

This mode of gene expression is especially exploited in germ cell fate decisions and during oogenesis, when the developing oocytes stockpile hundreds of different mRNAs required for early embryogenesis.

In the Caenorhabditis elegans one-cell embryo, while the actomyosin cytoskeleton is required for asymmetric localization of the PAR proteins, anterior PAR proteins exert a feedback regulation on contractility.

Originally identified in Drosophila and C. elegans where the Scribble complex was found to work with the Par-based and Crumbs-based polarity modules to regulate apicobasal polarity and asymmetry in cells and tissues during embryogenesis, their mammalian homologs have all been identified in recent years.

Autophagy is also required for the removal of extra P-granule (germ granules in C. elegans) components in somatic cells of early embryos and thereby for the specific distribution of P-granules to germ cells.

Here, we show that CSP-1 is a pro-apoptotic caspase that promotes programmed cell death in a subset of cells fated to die during C. elegans embryogenesis. csp-1 is expressed robustly in late pachytene nuclei of the germline and is required maternally for its role in embryonic programmed cell deaths.

In culture, the ability of pluripotent cells from the embryo to respond to the FGF and activin/nodal-like mesoderm-inducing pathways is compromised following inhibition of lin28 function.

Using Caenorhabditis elegans as a model system we show that the THO complex is essential for mitotic genome integrity and the developmentally regulated mitotic cell cycles occurring during late postembryonic stages.

Both lin28a and lin28b are expressed in pluripotent cells of the Xenopus embryo and are enriched in cells that respond to mesoderm-inducing signals.

The PAR clan of polarity regulating genes was initially discovered in a genetic screen searching for genes involved in asymmetric cell divisions in the Caenorhabditis elegans embryo.

The restricted spatiotemporal translation of maternal mRNAs, which is crucial for correct cell fate specification in early C. elegans embryos, is regulated primarily through the 3'UTR.

Previously we have identified a series of cellular miRNA molecules up- or down-regulated in infectious bursal disease virus (IBDV) infected chicken embryo fibroblasts and Bursa of Fabricius with gene microarray analysis.

Here we showed that loss of function mutations in 19 genes acting at overlapping or distinct stages of autophagy caused increased numbers of cell corpses in C. elegans embryos.

Here, we identify Artichoke (ATK), an evolutionarily conserved leucine-rich repeat ECM protein that is required for normal morphogenesis and function of ciliated sensilla in Drosophila. atk is transiently expressed in accessory cells in all ciliated sensory organs during their late embryonic development.

As a result, single cells of C. elegans embryos as early as the 2-cell stage and single neurons in ganglia can be induced to express genes selectively.

In this study, we found that it was a guanine nucleotide exchange factor and induced both cell migration in a cultured embryonic fibroblast cell line and cell invasion in cancer cell lines; moreover, it was observed to promote anchorage-independent growth in oral cancer cells.

By combining these techniques with live-cell imaging, we showed that an essential embryonic gene, Coronin, which is associated with human neurobehavioral dysfunction, regulates actin organization and cell morphology during C. elegans postembryonic neuroblast migration and neuritogenesis.

DEPDC1B was a guanine nucleotide exchange factor and induced both cell migration in a cultured embryonic fibroblast cell line and cell invasion in cancer cell lines; moreover, it was observed to promote anchorage-independent growth in oral cancer cells.

Spindle positioning is an imperative cellular process that regulates a number of different developmental events throughout embryogenesis.

In Caenorhabditis elegans, the first germ cell is established when RNA and protein-rich P granules localize to the posterior of the one-cell embryo.

It is critical that the cell movements of gastrulation be precisely controlled, and coordinated with cell specification, in order for the embryo to develop normally.

The asymmetric cell division process is required for cellular differentiation and embryonic development.

The anoxia-induced shift of cells from an actively dividing state to an arrested state reveals a previously uncharacterized prophase checkpoint in the C. elegans embryo.

Recent studies have demonstrated a correlation between cell size and the behaviors of the cytoskeletal division machinery during embryogenesis, giving insight into how a core cellular process is modulated over the course of development.

For example, we predict that a cell polarity module was altered during the evolution of the Protorhabditis group and show that PAR-1, a kinase localized asymmetrically in C. elegans early embryos, is symmetrically localized in the one-cell stage of Protorhabditis group species.

We have revealed that in Caenorhabditis elegans, non-sulfated chondroitin is required for normal cell division and cytokinesis at an early developmental stage, whereas heparan sulfate is essential for embryonic morphogenesis in the later stages of development.

We describe a mechanism that prevents precocious mitosis in germ cells undergoing meiosis, propose that this mechanism maintains germ cell identity by delaying the onset of embryonic gene activation until after fertilization, and provide a paradigm for the possible origin of human teratomas.

Furthermore, we provide evidence, by monitoring seam cell lineage, that one of the checkpoint genes is required for proper postembryonic cell proliferation.

CeR-2 is expressed in most cells from the early embryo to adult stages.

In one-cell stage C. elegans embryos, this process is accompanied by asymmetric spindle positioning, which is regulated by anterior-posterior (A-P) polarity cues and driven by force generators located at the cell membrane.

Here, we provide evidence that a population of dynein, which is located on intracellular organelles and is responsible for organelle transport toward the centrosome, generates the force required for centrosome centration in Caenorhabditis elegans embryos.

In Caenorhabditis elegans, the one-cell embryo is transcriptionally inactive, but at around eight-cell stage transcription is activated in the somatic lineage.

Here, we show that the leucine-rich repeat protein LRR-1 promotes cell cycle progression during C. elegans development, both in the germ line and in the early embryo.

A cell-specific microarray profiling study revealed a set of transcription factors that are highly expressed in embryonic C. elegans GABAergic neurons.

Significantly, in vivo structure-function analysis establishes a role for the F-BAR domain in promoting rapid and robust cell adhesion during embryonic closure events, independent of the Rho guanosine triphosphatase-activating protein domain.

In the one-cell Caenorhabditis elegans embryo, dynein is required for spindle-pulling forces during mitosis.

Cytoplasmic incompatibility induced by inherited intracellular bacteria of arthropods, and Medea elements found in flour beetles, are both forms of postsegregation distortion involving the killing of embryos in order to increase the ratio of progeny that inherit them.

Intercellular communication plays a pivotal role in regulating and coordinating oocyte meiosis and fertilization, key triggers for embryonic development.

We suggest that novel Sm RNPs directly or indirectly influence posttranscriptional control of maternal mRNAs to promote germ cell specification in the early C. elegans embryo.

Wnt signaling is one of the most important developmental signaling pathways that controls cell fate decisions and tissue patterning during early embryonic and later development.

Here, we show that Sm proteins also regulate germ cell specification during early C. elegans embryogenesis.

In the C. elegans one-cell embryo Arp2/3 promotes the establishment of anterior/posterior polarity and promotes MT growth that propels the anterior migration of the male pronucleus.

Using specific mutants that are deficient for ark function, we demonstrate that ARK is essential for most programmed cell death (PCD) during D. melanogaster development, as well as for radiation-induced apoptosis. ark mutant embryos have extra cells, and tissues such as brain lobes and wing discs are enlarged.

We also describe methods for in vitro RNA interference, fluorescence-activated cell sorting of embryo cells and imaging of cultured cells for patch-clamp electrophysiology studies.

MRG15, a mammalian protein related to the mortality factor MORF4, is required for cell proliferation and embryo survival.

While screening for genes that affect the ability of the intestinal cells to appropriately make this cell cycle transition during post-embryonic development, we isolated mutants that either compromise this switch and remain mononucleate, or cause these cells to undergo multiple rounds of nuclear division.

In the MAPCeL (Microarray Profiling C. elegans cells) method, we used fluorescence activated cell sorting (FACS) to isolate GFP-tagged embryonic neurons for microarray analysis.

Galpha is required for asymmetric spindle positioning in the one-celled embryo.

Recent work has revealed an evolutionarily conserved trio of proteins that regulate cell polarity in epithelial cells, embryonic blastomeres and neural precursors.

Suppressing endogenous PAR-1 function inhibits Wnt signalling through beta-catenin in mammalian cells, and Xenopus and Drosophila embryos.

Previous work has shown that GPB-1, the Gbeta subunit of a heterotrimeric G protein, is required for orientation of early cell division axes in C. elegans embryos.

Here we show that Spalt works as a cell fate switch between two EGFR-induced cell types, the oenocytes and the precursors of the pentascolopodial organ in the embryonic peripheral nervous system.

Wnt signaling has been demonstrated to regulate diverse cell processes throughout the development of the Caenorhabditis elegans embryo.

In dividing preneural cells at the ventricular (luminal) surface of the embryonic telencephalon, ASIP localize in adherence junctions of luminal surface regardless of the axis of cell division.

Moreover, disruption of Sm activity caused defects in P granule localization to the germ cell precursors during early embryogenesis.

The gene is expressed in germ cells and all somatic cells of the embryonic to adult stage.

Promoter analysis of the CE2FT-1 gene using green fluorescent protein reporter constructs demonstrates that CE2FT-1 is expressed in single cells of early stage embryos and exclusively in the 20 intestinal cells of L(1)-L(4) and adult worms.

Work from my laboratory in the last 5 years has shown that teratogens, such as hyperthermia, 4-hydroperoxycyclophosphamide, and staurosporine, induce cell death in day 9 mouse embryos by activating the mitochondrial apoptotic pathway, i.e., mitochondrial release of cytochrome c, activation of caspase-9 and -3, inactivation of poly (ADP-ribose) polymerase (PARP), and systematic degradation of DNA.

We found that the phosphorylation state of histone H3 and cell cycle-regulated proteins recognized by the MPM-2 antibody were not detectable in anoxic embryos.

The PAR proteins are required for polarity and asymmetric localization of cell fate determinants in C. elegans embryos.

These results indicate that genome-wide repression via a nanos-regulated, germ cell-specific chromatin organization is a conserved feature of germline maintenance during embryogenesis.

A recent study has now shown that differential cell-cycle timing in the first cell divisions of the Caenorhabditis elegans embryo is in part controlled by a DNA replication checkpoint.

To determine the basis of the net force imbalance that causes spindle displacement in one-cell Caenorhabditis elegans embryos, we fragmented centrosomes with an ultraviolet laser.

We studied the phenotypes produced by RNAi-induced downregulation of gp210 in both human (HeLa) cells and Caenorhabditis elegans embryos.

Immunolocalization revealed that ANTR2 was expressed in the leaf mesophyll cells as well as in the developing embryo at the upturned-U stage.

In Caenorhabditis elegans, MTA1-like genes regulate cell polarity, migration, embryonic patterning, and vulva development.

Programmed cell death is the physiological process responsible for shaping organs during embryogenesis, maintaining tissue homeostasis and allowing controlled deletion of potentially harmful cells within the adult organism.

Heterotrimeric G proteins promote microtubule forces that position mitotic spindles during asymmetric cell division in C. elegans embryos.

Mutation of this domain not only prevents ciliary localization but also eliminates Smo activity both in cultured cells and in zebrafish embryos.

Here we address this problem in a screen designed to identify all genes required for the first two rounds of cell division in the Caenorhabditis elegans embryo.

Since cell death regulation is tightly interwoven with cell cycle and checkpoint controls, and embryos of the fly, fish and frog exhibit unique embryonic cell cycle regulation, it is of great interest to understand how early embryos coordinate these cellular functions.

Our analysis indicates that spindle checkpoint mechanisms are functional in the rapidly dividing cells of an early animal embryo and that this checkpoint can prevent chromosome segregation defects during mitosis.

Although the spindle checkpoint can be activated in many different cell types, the role of this regulatory mechanism in rapidly dividing embryonic animal cells has remained controversial.

RNA interference-mediated down-regulation of Ce-BAF caused gross defects in chromosome segregation, chromatin decondensation, and mitotic progression as early as the two-cell stage, and embryos died at the approximately 100-cell stage.

Consistently, EYA-1 was expressed in the nuclei of a subset of anterior cells including pharyngeal and body wall muscle cells, starting from the morphogenesis stage in embryogenesis.

Mutations at the flightless-I locus (fliI) of Drosophila melanogaster cause flightlessness or, when severe, incomplete cellularization during early embryogenesis, with subsequent abnormalities in mesoderm invagination and in gastrulation.

During the first cell cycle, P granules, cytoplasmic components that are segregated to the germ-line, are localized to the posterior of the embryo.

Cell-cell interactions in the nematode embryo can be inhibited with polysulfated hydrocarbon dyes (e.g.

Homeobox-containing genes are a phylogenetically widespread family of transcription factors that can regulate cell fates during embryogenesis.

In a 4-cell stage C. elegans embryo, signaling by the P2 blastomere induces anterior-posterior polarity in the adjacent EMS blastomere, leading to endoderm formation.

Using this assay, we have identified 48 mutations in 34 loci which are required for specific cell division processes in the one cell stage embryo.

The O/E proteins are expressed in cells of the olfactory neuronal lineage throughout development and are also expressed transiently in neurons in the developing nervous system during embryogenesis.

To identify novel components required for cell division processes in complex eukaryotes, we have undertaken an extensive mutational analysis in the one cell stage Caenorhabditis elegans embryo.

Floor plate cells secrete a diffusible factor called 'netrin', that promotes the outgrowth of axons in the embryonic chick brain.

Loss of function of the gamma-tubulin gene by RNAi induces a strong polyploidization of mitotic germ cells and embryos, but does not affect meiosis and pronuclear migration.

Here, the evidence that interactions control division orientation in some cells of the early C. elegans embryo is presented, and what is known about how contact can regulate division orientation is discussed.

These phenotypes were well correlated with mRNA expression localized in the meiotic cells of gonad and early embryonic cells.

Our results indicate that these genes represent most of the genes on chromosome III that are required for proper cell division in C. elegans embryos.

Exopher formation (exopheresis) by BWM is sex-specific and a non-cell autonomous process regulated by developing embryos in the uterus.

By leveraging the precisely mapped cell lineage at single cell resolution, we are able to study at a systems level how early embryonic cells communicate across morphogenetic domains for the coordinated processes of gene expressions and collective cellular behaviors that regulate tissue morphogenesis.

After acquisition, SAC strength, which manifests as the degree of mitotic lengthening induced by spindle perturbations, is specific to different cell types and is modulated by cell size, showing similarity to SAC control in early Caenorhabditis elegans embryos.

A molecular understanding of heterochrony was first established by genetic mutant analysis in the nematode C. elegans, revealing a genetic pathway that controls the proper timing of cellular patterning events executed during distinct postembryonic juvenile and adult stages2.

BM regulates PGC quiescence even though PGCs are enwrapped by somatic niche cells and do not contact the BM; this can be demonstrated by depleting laminin, which causes normally quiescent embryonic PGCs to proliferate.

We next review the key factors and pathways that regulate the specification of discrete cells and lineages during embryogenesis and postembryonic development; we focus on transcription factors and include numerous lineage diagrams that depict the expression of key factors that specify embryonic founder cells and postembryonic blast cells, and the diverse somatic cell fates they generate.

ATGL, the rate-limiting lipase in cellular lipolysis, is expressed and required in the hypodermis to regulate mitochondrial function and support embryogenesis.

Reproductive cues modulate this decline in cellular proteostasis to influence organismal stress resilience in Caenorhabditis elegans We previously uncovered a pathway that links the integrity of developing embryos to somatic health in reproductive adults.

We also show that a balance between Cyclin B-Cdk1 and PP2A-B55 activity, regulated by KIN-4, is essential to ensure asynchronous cell divisions in the early worm embryo.

Here, we present a systematic single-cell comparison of embryogenesis between de novo-induced tetraploid and diploid C. elegans embryos, integrating live imaging, lineage tracing, phenotypic quantification, and transcriptomic profiling.

We employed Nutlin-3a, a reversible inhibitor of the P53/MDM2 interaction, to induce cellular senescence in human embryonic lung fibroblast MRC-5 cells, followed by DMB treatment to evaluate its antagonistic effects.

In humans, bystin promotes cell adhesion and invasion in gliomas, and, with its binding partner trophinin, triggers embryonic implantation into the uterine wall.

Combining ChIP-seq data with single-cell RNA-seq data in a machine-learning model identifies TFs with a prominent role in promoting target gene expression in specific cell types, even differentiating between parent-daughter cells during embryogenesis.

Many RBP genes are expressed in a cell type- and developmental stage-specific manner in the embryo, emphasizing that RBPs can contribute to distinct gene expression patterns.

Many RNA-binding protein genes are expressed in a cell type- and developmental stage-specific manner in the embryo, emphasizing that RNA-binding proteins can contribute to distinct gene expression patterns.

Finally, we present the application of this method to investigate the orientation of cellular division axes that contributes to the regulation of spatial cellular patterning and cell fate specification in developing embryos.

Calreticulin (CRT), a Ca(2+)-binding protein known to have many cellular functions, including regulation of Ca(2+) homoeostasis and chaperone activity, is essential for heart and brain development during embryogenesis in mice.

Both of the TFAR15 mRNA and protein were highly expressed in TF-1 cells after GM-CSF withdrawal.In vitro analysis showed that the recombinant TFAR15 protein could inhibit the natural cell death of 293 cells, an embryonic kidney cell line.

The effect of NF-kappaB on paclitaxel-sensitivity appears to be specific to cancer cells because normal fibroblasts derived from embryos lacking p65 subunit of NF-kappaB and wild type littermate embryos were insensitive to paclitaxel-induced G2/M cell cycle arrest.

We have found that genes encoding putative deubiquitylating enzymes (DUBs) are required for polarization of one-cell embryos.

These data suggest that two GATA factors that are required for seam cell specification in the embryo independently of Wnt signaling are reused downstream of Wnt signaling to maintain the progenitor fate during stem cell-like divisions in larval development.

Our studies suggest that PRC2 represses the X chromosomes in Caenorhabditis elegans germ cells, and this repression is transmitted to embryos by both sperm and oocytes.

We have recently demonstrated that the putative neurotoxin receptor lat-1 defines a mechanism required for the alignment of cell division planes in the early embryo of the nematode C. elegans.

However, studies from plant cells, cultured neurons, and nematode embryos suggest that katanin could be required for the organization or postnucleation processing of microtubules, rather than the dissolution of microtubule structures.

Deficiencies in this last class suggest that the cell death program does not require normal embryonic cell proliferation to be activated and suggest that while some genes required for cell division might also be required for cell death, others are not.

The analysis of the development of these mutants suggests that the clock controlling the cell cycles in the early embryo is directly coupled to the fate of a cell and that there must be another developmental clock that activates the determinative inventory for the early decision-making.

This suggests that ceh-18 affects, directly or indirectly, a sheath cell signal that causes oocytes to maintain diakinesis arrest. ceh-18 also participates in directing gonad migration and in specifying the differentiated phenotypes of epidermal cells during postembryonic development.

The cubitus interruptus (ci) gene of Drosophila is expressed in all anterior compartment cells in both embryos and imaginal disks where it encodes a putative zinc-finger protein related to the vertebrate Gli and C. elegans Tra-1 proteins.

Taken together, these results suggest that germ-cell fate depends on an inhibitory mechanism that blocks new gene expression in the early embryonic germ lineage.

In this study, we developed a computational framework for the exploration of the morphogenetic domain cell signaling networks that may regulate C. elegans gastrulation and embryonic organogenesis.

It was assumed that the drug might have some effect on the chromosomes or genes in the germinal stem-cell of the heartworm and interfere with protein syntheses, resulting in inhibition of embryonic development.

The general functions of the family appear to be the cell-type-specific stimulation of proliferation and the suppression of terminal differentiation during embryonic development.