Histological studies on embryonic development of the rabbit heart

2003 ◽  
Vol 51 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Emese Balogh ◽  
P. Sótonyi

Two experiments were performed to evaluate the normal development of the rabbit heart. In the first experiment the most intensive period of heart development was determined in rabbit embryos. The second experiment studied the most intensive period of heart development, determined in the first experiment, by concentrated sampling at 8-hour intervals. After cutting open the uterine wall opposite the discoid placenta, rabbit embryos were removed from the ampullae of the uterus using capillary tubes, under stereomicroscope at fivefold magnification. The embryos were subsequently placed into 4% formalin solution for 24 h. After fixation, slides stained with haematoxylin and eosin were made for histological examination. In the first experiment 51 embryos were examined, while during the second experiment a total of 113 embryos, representing different stages of development, were collected. Finally the data obtained on rabbits were compared with the well-known development of the heart in humans and mice.

Zygote ◽  
2012 ◽  
Vol 21 (4) ◽  
pp. 385-393
Author(s):  
Manjula Brahmajosyula ◽  
Masashi Miyake

SummaryArginine modification to citrulline (citrullination) is catalyzed by peptidylarginine deiminases (PADs) and one of the isomers PAD4 is shown to be involved in the gene regulation. In our previous paper we studied the localization and expression of PAD4 and the target of PAD4 in mammalian gametes and preimplantation embryos. In this study the role of PAD4 was examined in the pig diploid parthenogenetic preimplantation embryonic development. Knockdown of PAD4 by RNAi resulted in delayed development. Inhibition of PAD4 by a potent PAD4 inhibitor Cl-amidine from the time of activation for 24 h resulted in developmental arrest at the first cleavage. Inhibition at the later stages of development resulted in delayed or arrested development. A shorter exposure to Cl-amidine for 6 h at any stage of growth resulted in slow development. Thus, this study suggests that PAD4 activity is essential for the normal development of the embryos.


Author(s):  
Scott Gilbert

This chapter looks at the beginnings of embryonic development, the function of embryonic stem cells. The development of the human embryo strikes both scientists and laypeople alike with awe and mystery. However, there is no consensus among scientists as to when the fetus becomes a “person.” This chapter will discuss these various stages of development and why different groups of scientists reason that they might be the basis for “personhood.”


Development ◽  
1973 ◽  
Vol 29 (2) ◽  
pp. 267-281
Author(s):  
G. Teitelman

Removal of the polar lobe at the trefoil stage of the first cleavage division of Ilyanassa embryos causes abnormalities much later in development. To determine if the developmental differences between normal and delobed embryos were reflected in alterations in protein synthesis and at what stages of development these become evident, protein solutions were separated by disc electrophoresis on basic acrylamide gels. For the analysis of the newly synthesized proteins, two protein samples, one labelled with 14C and the other with 3H, were combined in the same electrophoretic column. Each was prepared from normal embryos or lobeless embryos at different stages of development. The distribution of the two groups of differentially labelled proteins was compared by a determination, for each fraction, of the ratio of the normalized 3H/14C counts for that particular fraction (R = 3H/14C). The plot of R versus fraction number was studied for various combinations of samples. During normal development the profile of labelled proteins remains unchanged until the onset of visible differentiation. At this stage, around day 4 of development, there are changes in biosynthesis revealed by a greater emphasis on the synthesis of slow moving proteins. The profile of labelled proteins of lobeless embryos remains unchanged up to the 5th day of development. This result is correlated with the absence, in the lobeless embryos, of many of the visible differentiations. Preliminary studies revealed that the spectrum of labelled proteins of the polar lobe is identical to the one present in lobeless embryos and in normal embryos in early stages of development. This suggests the possibility that the morphogenetic factors associated with the polar lobe are not among the newly synthesized proteins. A hypothesis is presented to account for the effects on morphogenesis and protein synthesis which are produced by removal of the polar lobe.


1989 ◽  
Vol 92 (2) ◽  
pp. 137-146 ◽  
Author(s):  
D.M. Glover

Drosophila is an attractive organism in which to study both the rapid rounds of mitosis typical of embryonic development in many species, and the longer cell cycles of diploid tissues later in development. Mutations in genes essential for mitosis in Drosophila may result in lethality in late embryonic, larval or pupal stages of development. In addition, mutations in many genes required for the nuclear divisions of early embryogenesis have been found in screens for female sterility. The mitotic mutations have phenotypes indicative of lesions at a variety of mitotic stages. A combined molecular and genetic analysis of these genes has the potential to unravel the complex set of protein-protein interactions that occur in this dynamic process.


Development ◽  
1998 ◽  
Vol 125 (6) ◽  
pp. 1037-1048 ◽  
Author(s):  
E. Kurant ◽  
C.Y. Pai ◽  
R. Sharf ◽  
N. Halachmi ◽  
Y.H. Sun ◽  
...  

The homeotic genes of the bithorax complex are required, among other things, for establishing the patterns of sensory organs in the embryonic peripheral nervous system (PNS). However, the molecular mechanisms by which these genes affect pattern formation in the PNS are not understood and other genes that function in this pathway are not characterized. Here we report the phenotypic and molecular analysis of one such gene, homothorax (hth; also named dorsotonals). Mutations in the hth gene seem to alter the identity of the abdominal chordotonal neurons, which depend on Abd-A for their normal development. However, these mutations do not alter the expression of the abd-A gene, suggesting that hth may be involved in modulating abd-A activity. We have generated multiple mutations in the hth locus and cloned the hth gene. hth encodes a homeodomain-containing protein that is most similar to the murine proto-oncogene meis1. The hth gene is expressed throughout embryonic development in a spatially restricted pattern, which is modulated in abdominal segments by abd-A and Ubx. The spatial distribution of the HTH protein during embryonic development is very similar to the distribution of the Extradenticle (EXD) protein, a known modulator of homeotic gene activity. Here we show that the PNS phenotype of exd mutant embryos is virtually indistinguishable from that of hth mutant embryos and does not simply follow the homeotic transformations observed in the epidermis. We also show that the HTH protein is present in extremely low levels in embryos lacking exd activity as compared to wild-type embryos. In contrast, the EXD protein is present in fairly normal levels in hth mutant embryos, but fails to accumulate in nuclei and remains cytoplasmic. Ectopic expression of hth can drive ectopic nuclear localization of EXD. Based on our observations we propose that the genetic interactions between hth and exd serve as a novel mechanism for regulating homeotic protein activity in embryonic PNS development.


Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 2065-2075 ◽  
Author(s):  
W. Wurst ◽  
A.B. Auerbach ◽  
A.L. Joyner

During mouse development, the homeobox-containing gene En-1 is specifically expressed across the mid-hindbrain junction, the ventral ectoderm of the limb buds, and in regions of the hindbrain, spinal cord, somites and somite-derived tissues. To address the function of En-1 during embryogenesis, we have generated mice homozygous for a targeted deletion of the En-1 homeobox. En-1 mutant mice died shortly after birth and exhibited multiple developmental defects. In the brains of newborn mutants, most of the colliculi and cerebellum were missing and the third and fourth cranial nerves were absent. A deletion of midhindbrain tissue was observed as early as 9.5 days of embryonic development and the phenotype resembles that previously reported for Wnt-1 mutant mice. In addition, patterning of the forelimb paws and sternum was disrupted, and the 13th ribs were truncated. The results of these studies suggest a cell autonomous role for En-1 in generation and/or survival of mid-hindbrain precursor cells and also a non-cell autonomous role in signalling normal development of the limbs and possibly sternum.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Sarah E Wetzel-Strong ◽  
Manyu Li ◽  
Toshio Nishikimi ◽  
Kathleen M Caron

The multi-functional peptide adrenomedullin ( Adm = gene, AM = protein) plays important roles in embryonic development and disease. Previous studies demonstrated that Adm knockout mice die at embryonic day 13.5 with small, disorganized hearts and hypoplastic lymphatic vessels, highlighting the importance of this peptide in normal cardiovascular development. Since Adm knockout animals are embryonic lethal, our goal was to generate and characterize a novel model of Adm over-expression to study the role of Adm during development and disease processes. Through gene targeting techniques, we generated a novel mouse model of Adm over-expression, abbreviated as Adm hi/hi . When we assessed gene expression of Adm from 10 different tissues, we found Adm hi/hi mice express 3- to 15-fold more Adm than wildtype littermates. Additionally, peptide levels of AM in lung and kidney, as well as circulating plasma levels of AM were elevated 3-fold over wildtype mice, indicating a functional increase in AM. Our initial analysis revealed that adult Adm hi/hi mice have larger heart weight to body weight ratios than wildtype littermates (4.93±0.23 vs. 5.96±0.29, n = 11-12). We found that compared to wildtype, Adm hi/hi embryos have more proliferating cells during heart development (14.46±1.11 vs. 31.97±2.84, n=4), indicating that hyperplasia drives Adm hi/hi heart enlargement. By crossing the Adm hi/hi line to different tissue-specific Cre lines, we were able to excise the stabilizing bovine growth hormone 3’UTR, thereby returning Adm expression levels back to wildtype in cells with active Cre recombinase. Using this approach, we identified the epicardium as a major source of AM during cardiac development. In conclusion, we found that AM derived primarily from the epicardium drives cardiac hyperplasia during embryonic development resulting in persistent, enlarged hearts of adult Adm hi/hi mice. Since our Adm hi/hi mice recapitulate the 3-fold plasma elevation of AM observed during human disease, this mouse line will be a useful tool for studying the role of elevated AM during disease.


2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Brian Thompson ◽  
Nicholas Katsanis ◽  
Nicholas Apostolopoulos ◽  
David C. Thompson ◽  
Daniel W. Nebert ◽  
...  

AbstractRetinoic acid (RA) is a potent morphogen required for embryonic development. RA is formed in a multistep process from vitamin A (retinol); RA acts in a paracrine fashion to shape the developing eye and is essential for normal optic vesicle and anterior segment formation. Perturbation in RA-signaling can result in severe ocular developmental diseases—including microphthalmia, anophthalmia, and coloboma. RA-signaling is also essential for embryonic development and life, as indicated by the significant consequences of mutations in genes involved in RA-signaling. The requirement of RA-signaling for normal development is further supported by the manifestation of severe pathologies in animal models of RA deficiency—such as ventral lens rotation, failure of optic cup formation, and embryonic and postnatal lethality. In this review, we summarize RA-signaling, recent advances in our understanding of this pathway in eye development, and the requirement of RA-signaling for embryonic development (e.g., organogenesis and limb bud development) and life.


2018 ◽  
Vol 54 (2) ◽  
pp. 154
Author(s):  
IN MAGRAS ◽  
Th.C. Tsiligianni

The aim of the present bibliographical review was to approach the most considerable causes, in relation to the unbridled pollution of innumerable areas of our planet. Congenital malformations are created during the prenatal development and could possible cause embryonic death. They become visible after an abortion or after the birth and they could be mild or extensive malformations. Monsters always stimulate the people’s interest and they were source of superstitions and topic of scientific research as well. In the international bibliography, there are plenty of such cases, and some of them are indicatively referred in the present review. The investigation of the causes of the congenital malformations is of a particular importance, in order to take the necessary preventive measures, when it is possible. The factors, which are responsible for the congenital malformations, are characterized as teratogenic or, in some cases, as embryo- or fetotoxic factors, and usually affect the genital cells of the parents or the organs of the pregnant female. A very important role in the mammalian congenital malformation play, except of the teratogenic factors, the animal species, the placenta type, the histochemical background of the mother and the embryo as well as the stage of the prenatal development during the exposition to the teratogenic factor. The teratogenic factors can be genetic or environmental. During the prenatal development, there is an interaction between the genome, which insure the genotypic feature of the species and the different epigenetic process, which create the phenotypic varieties. The interaction of the genome with the microenvironment, where the embryo is developed, is usually the key of the congenital malformation. Every genetic disturbance leads to the deviation from the normal development, because the embryonic development is depended on the genome. Genetical disturbance is possible to arise because of some chromosomal atypical or abnormal genes or (endo - or - exogenous) environmental factors. The environmental factors are numerous and according to their nature they can be classified to the following categories: physical factors, chemical agents and biological agents. Physical factors are the ionizing and the non - ionizing radiations. A new type of environmental pollution has been raised, after the artificial production of the radiations. A very important role in the increase of the cases of congenital malformation play the ionizing radiation, as a free nuclear energy after the bombing, the nuclear accidents and the nuclear litter. The ionizing radiation, as well as the radiowaves and the microwaves, known as radiofrequency or radiomagnetic radiation, include low energy. Their radio-embryo-toxicity is not negligible, however, and depends on the area of the spectrum, the power density, the "special absorption rate", the duration of the exposure, the sensitivity of the embryo fetus and its organs. A lot of chemical substances adversely intervene in the normal embryonic and fetal development, causing congenital malformations. These substances could be natural having their origin from the external environment or from the organism itself or they could be artificial. Most of the drugs are considered as suspicious teratogens. Some plants contain dangerous embryotoxical substances and pregnant animals must not consume them. The deficiency of some nutrients is possible to cause disturbances in the prenatal development. Moreover, congenital malformations are observed after the deficiency of some elements. Infection agents, such as viruses, bacteria, protozoa, fungus and parasites, when they pass through the placental barrier are possible to cause congenital malformations. Also, the vaccination of the pregnant animals has to be avoided or to be applied on a period that is not critical for teratogenesis. Furthermore, there are a lot of unknown teratogenic agents that usually cause a considerable rate of congenital malformations. During the early embryonic development, there is a "critical period" where the embryo is particularly sensitive in the teratogenic agents. It is obvious that, if any teratogenic agent affects the embryonic development during the "critical period", the normal development of the embryo will be disorganized resulting in the embryonic deformities. In the full text of this review a detailed analysis of what can happen during this period is discussed. In the second half of the former century, the frequency of the congenital malformations has been considerably increased in human being and in animals, as well. This phenomenon is supported by a series of real events and situations, such as: the uncontrolled use of the nuclear energy and the nuclear accidents, the pollution by the major as well as the minor polemic conflicts, the unrestrained industrial development, the production of an enormous number of chemical substances, the increase of the fumes, the uncontrolled spreading of the electromagnetic radiation, the over consumption of industrial elaborated aliments, the malnutrition, the overexploitation of the land, with an excess of chemical fertilizing, pesticides and plant hormons, as well as the irresponsible use of hormones, drugs and unusual feed for livestock. The restriction of the continuing pollution and the simultaneous recovery of the environment must be the target of the humanity. The protection of the environment, beyond the improvement of health generally and the welfare of the animals and human will contribute in the diminuition of the congenital malformation cases in newborn animals and in human, as well.


1998 ◽  
Vol 19 (4) ◽  
pp. 345-355 ◽  
Author(s):  
S. Tripepi ◽  
F. Rossi ◽  
G. Peluso

AbstractThe embryonic development of Triturus italicus was observed at different temperatures. Normal development occurred between 10°C and 22.5°C. In this range of temperatures an hyperbolic relationship between development time and temperature was confirmed.


Sign in / Sign up

Export Citation Format

Share Document