MicroRNA processing machinery in the developing chick embryo

In the developing vertebrate heart, cells that contribute to vascular smooth muscle, cardiac fibroblasts, and coronary endothelial cells are derived from the proepicardium and associated cells originally located at the venous pole of the primitive heart tube. Recently, there has been much interest in the regulatory mechanisms that control epicardium-derived cell (EPDC) lineage development and mobilization with adult cardiac injury. However, less is known of the embryonic origins and inductive mechanisms that control the initial induction of the proepicardium. The study by Schlueter and Brand1 in the current issue of Circulation Research reports fate mapping of proepicardial progenitors to the somatic mesoderm and demonstrates a critical role for the basic helix-loop-helix transcription factor Twist1 in the earliest stages of proepicardial development. Article, see p 1128 The heart is the first organ to function in the developing vertebrate embryo, and beating of the primitive heart tube is apparent by embryonic day (E)8 in mouse and by 40 hours of development in chicken embryos.2 As the primitive heart tube loops, lateral plate mesoderm cells on the right side of the embryo at the cardiac venous pole begin to form the proepicardium.3 Schlueter and Brand1 demonstrate through fate mapping studies in avian embryos that at least some cells of the proepicardium are derived from the somatic layer of lateral plate mesoderm. The somatic compartment (somatopleure) of the lateral plate mesoderm is adjacent to the ectoderm and forms the body wall.4 The new data provide initial evidence that cells of the proepicardium also are derived from somatic mesodermal layer. The proepicardium shares many characteristics with other mesothelia of the major coelomic organs that contribute progenitors of fibroblasts and smooth muscle to the lung, gut, kidney, etc.4 The embryonic origins of coelomic mesothelia are not …

The present study was conducted to determine the adverse effects of high incubation temperature on growth, development and genome stability of broiler chick embryo in ovo). One hundred twenty broiler eggs from Cobb Company, USA were weighted and divided into two groups. The first group was incubated at 37oC ± 0.5oC, and the second group was incubated at 41oC ± 0.5oC from 0 to 18th day. Starting on day 4th and every other day; three eggs from each group were examined following performed measurements as weight of eggs post incubation, embryo, yolk, and egg shell for measuring growth index. Blood smear was also prepared for counting heterophiles, and lymphocytes to determine H/L ratio. Micronucleus formation and presence of binucleated red blood cells were investigated as genome stability parameters, in 2000 cells. Significant reduction (P<0.01) in growth indices was observed in embryos grown at 41oC compared to those grown at 37oC ± 0.5oC. Reduction in H/L ratio was statistically significant (p≤0.01) in embryos of 2nd group comparing to 1st group embryos. Blood of embryo from heat stress group group (2) showed Red blood cells with micronuclei and binucleated cells while no such phenomenon could be seen in embryos from control group group (1). These results suggested that heat stress is influencing cell division at telophase and induces chromosomal damage. 88% of chicks from group (1) were hatched on day 21st; only 18% of chicks from group (2) were hatched lately on day 23rd, while the others were found dead. These results indicate that heat stress not only adversely affects growth and development of embryo stem cells but also induces genome instability which intern resulted in poultry production losses.

Cyclooxygenases (COXs) have important functions in various physiological and pathological processes. COX-2 expression is highly induced by a variety of stimuli and is observed during certain periods of embryonic development. In this report, the direct effect of COX-2 expression on embryonic development is examined in a novel COX-2 transgenic mouse model that ubiquitously expresses human COX-2 from the early stages of embryonic development. COX-2 transgenic fetuses exhibit severe skeletal malformations and die shortly after birth. Skeletal malformations are localized along the entire vertebral column and rib cage and are linked to defective formation of cartilage anlagen. The cartilage anlagen of axial skeleton fail to properly develop in transgenic embryos because of impaired precartilaginous sclerotomal condensation, which results from the reduction of cell number in the sclerotome. Despite the ubiquitous expression of COX-2, the number of apoptotic cells is highly increased in the sclerotome of transgenic embryos but not in other tissues, suggesting that it is a tissue-specific response. Therefore, the loss of sclerotomal cells due to an increased apoptosis is probably responsible for axial skeletal malformations in transgenic fetuses. In addition, the sclerotomal accumulation of p53 protein is observed in transgenic embryos, suggesting that COX-2 may induce apoptosis via the up-regulation of p53. Our results demonstrate that the aberrant COX-2 signaling during embryonic development is teratogenic and suggest a possible association of COX-2 with fetal malformations of unknown etiology.

Background: Vitamin A has potentially harmful effects on the development of chick embryos even at very low dose concentration. Vitamin A different doses cause embryotoxic and teratogenic effects on the developing of the chick embryo. Hence, due to teratogenicity of this vitamin it can be used with utmost caution during pregnancy. Methods: Fertile chicken eggs (obtained from local hatchery) were injected with three doses of Vitamin A (15 IU/ml, 30 IU/ml, 75 IU/ml) into the center of the egg yolk. Morphometric parameters as mortality rate, body weight (g), crown rump length (mm) of embryo and Frequency % of different anomalies gross malformations were measured. Whole chicken samples were taken by 4th, 8th and 18th incubation day. Daam, Hox and Tbx genes expression profile were analyzed. Result: Dose-dependent defects and embryo lethality in the chick embryos developed when exposed to higher concentrations. Our study record for the first time the duplication in the heart, brain and eye. Also showed duplication of the neck forming S-shaped showed in some malformed chick embryos. The three investigated genes showed different fluctuations confirming the malformations detected.

Effect of mobile phone induced electromagnetic fields on the development of chick embryo.

Metabolic control of pulmonary ventilation in the developing chick embryo.

Overlapping Roles and Collective Requirement for the Coreceptors GAS1, CDO, and BOC in SHH Pathway Function

Oscillating signaling pathways during embryonic development

FoxJ1 is a forkhead transcription factor expressed in multiple tissues during development and a major regulator of cilia development. FoxJ1(-/-) mice present with defects in odontogenesis, and we correlate these defects to hierarchical interactions between homeodomain factors Pitx2 and Dlx2 with FoxJ1 in regulating their expression through direct physical interactions. Chromatin immunoprecipitation assays reveal endogenous Pitx2 and Dlx2 binding to the Dlx2 promoter and Dlx2 binding to the FoxJ1 promoter as well as Dlx2 and FoxJ1 binding to the amelogenin promoter. PITX2 activation of the Dlx2 promoter is attenuated by a direct Dlx2 physical interaction with PITX2. Dlx2 autoregulates its promoter, and Dlx2 transcriptionally activates the downstream gene FoxJ1. Dlx2 and FoxJ1 physically interact and synergistically regulate both Dlx2 and FoxJ1 promoters. Dlx2 and FoxJ1 also activate the amelogenin promoter, and amelogenin is required for enamel formation and late stage tooth development. FoxJ1(-/-) mice maxillary and mandibular incisors are reduced in length and width and have reduced amelogenin expression. FoxJ1(-/-) mice show a reduced and defective ameloblast layer, revealing a biological effect of these transcription factor hierarchies during tooth morphogenesis. These transcriptional mechanisms may contribute to other developmental processes such as neuronal, pituitary, and heart development.

Generation of mutants with developmental defects in zebrafish by ENU mutagenesis

Botulinum toxin (BTX) is a potent neurotoxin produced by Clostridium botulinum and has wide usage in different areas. The current study aimed to analyze the effects of C. botulinum toxin on the central nerve system in chick embryos. Forty fertile Hubbard Broil eggs, all at Stage 8 of development, were divided into four equal groups: Group 1 embryos (n=10), the control group, were explanted and grown for 18 h in a nutrient medium (thin albumin). Group 2 embryos (n=10) were grown in medium containing 5 U BTX, Group 3 embryos (n=10) in a medium containing 10 U BTX and Group 4 embryos (n=10) in medium containing 20 U BTX. After the incubation period, 80% of Group 1 and 2 embryos and 90% of Group 3 and 4 embryos had intact neural tubes (P>0.05). The results of this study suggest that BTX had no additional effect on neural tube development in early chick embryos.

Environmental stress can affect the development of the embryo, including causing the death of the embryo. Environmental factors that can cause stress include salinity and zinc sulfate, zinc sulphate is a trace element and can affect embryonic development. The purpose of this study was to analyze the environment in Chicken embryonic development. A literature search was carried out systematically through the PubMed, NCBI, Google Scholar databases using keywords, namely, “heat, stress, embryo, chicken”. Based on these keywords, the articles obtained were first selected by setting several inclusion criteria. Articles that do not meet the inclusion criteria are eliminated, and articles that meet the criteria will be analysed to obtain data. Based on the search results 21326 articles were obtained, and 21 articles that meet the inclusion criteria were selected. The result above also showed that heat stress give impact to development of embryo. From the results of the research conducted, it can be concluded that the environment has an impact on the development of the embryo. Further studies are needed, especially those related to other types of stress that can affect embryonic development in various types of animals.

Supplemental L-arginine promotes hepatocyte proliferation and alters liver fatty acid metabolism in the late embryonic phase: an RNA-seq analysis

Sequential Acquisition of Transcriptional Control during Early Embryonic Development in the Rabbit

BackgroundThe FGF/Ras/Ral/RLIP pathway is required for the gastrulation process during the early development of vertebrates. The Ral Interacting Protein (RLIP also known as RalBP1) interacts with GTP-bound Ral proteins. RLIP/RalBP1 is a modular protein capable of participating in many cellular functions.Methodology/Principal FindingsTo investigate the role of RLIP in early development, a two-hybrid screening using a library of maternal cDNAs of the amphibian Xenopus laevis was performed. Xreps1 was isolated as a partner of RLIP/RalBP1 and its function was studied. The mutual interacting domains of Xreps1 and Xenopus RLIP (XRLIP) were identified. Xreps1 expressed in vivo, or synthesized in vitro, interacts with in vitro expressed XRLIP. Interestingly, targeting of Xreps1 or the Xreps1-binding domain of XRLIP (XRLIP(469–636)) to the plasma membrane through their fusion to the CAAX sequence induces a hyperpigmentation phenotype of the embryo. This hyperpigmented phenotype induced by XRLIP(469–636)-CAAX can be rescued by co-expression of a deletion mutant of Xreps1 restricted to the RLIP-binding domain (Xreps1(RLIP-BD)) but not by co-expression of a cDNA coding for a longer form of Xreps1.Conclusion/SignificanceWe demonstrate here that RLIP/RalBP1, an effector of Ral involved in receptor-mediated endocytosis and in the regulation of actin dynamics during embryonic development, also interacts with Reps1. Although these two proteins are present early during embryonic development, they are active only at the end of gastrulation. Our results suggest that the interaction between RLIP and Reps1 is negatively controlled during the cleavage stage of development, which is characterized by rapid mitosis. Later in development, Reps1 is required for the normal function of the ectodermic cell, and its targeting into the plasma membrane affects the stability of the ectoderm.