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PubMed1986

Destruction of the preganglionic nerves by beta-bungarotoxin does not interfere with normal embryonic development of the rat adrenal medulla.

Using beta-bungarotoxin (beta-BTX) as a tool to eliminate the preganglionic cholinergic nerve supply to the embryonic rat adrenal gland, we have investigated whether or not these nerves affect the differentiation of embryonic chromaffin cells (pheochromoblasts). Rat fetuses received a single injection of 1 or 2 micrograms beta-BTX or an identical volume of saline at embryonic day (E) 17 and were taken for morphological and biochemical analyses at E 21. Administration of beta-BTX caused a 15 to 20% reduction in body weight, crown-rump-length and adrenal weight. Spinal cord development was reduced and acetylcholinesterase-positive cells in ventral and lateral columns were virtually absent in toxin-treated animals. In adrenal glands, a decrease of choline acetyltransferase activity to 13% of control levels and a concomitant decrease of ultrastructurally identifiable nerve fibers and axon terminals revealed that application of 2 micrograms beta-BTX effectively reduced the neuronal input to E 21 adrenal glands. Values for total adrenal catecholamines, relative amounts of adrenaline and noradrenaline, tyrosine hydroxylase and phenylethanolamine N-methyltransferase activities were unaltered. All ultrastructural features of pheochromoblasts (except the lack of synapse-like axon terminals) were inconspicuous. Corticosterone levels in adrenals and plasma were identical to controls. These data strongly suggest that normal embryonic development of adrenal chromaffin cells does not require an intact nerve supply.

Adrenal Medulla↗
PubMed2002

FA composition of heart and skeletal muscle during embryonic development of the king penguin.

Since the yolk lipids of the king penguin (Aptenodytes patagonicus) naturally contain the highest concentrations of DHA and EPA yet reported for the eggs of any avian species, the effects of this (n-3)-rich yolk on the FA profiles of the embryonic heart and skeletal muscle were investigated. The concentrations (mg/g wet tissue) of phospholipid (PL) in the developing heart and leg muscle of the penguin doubled between days 27 and 55 from the beginning of egg incubation (i.e., from the halfway stage of embryonic development to 2 d posthatch), whereas no net increase occurred in pectoral muscle. During this period, the concentration of TAG in heart decreased by half but increased two- and sixfold in leg and pectoral muscle, respectively. The most notable change in cholesteryl ester concentration occurred in pectoral muscle, increasing ninefold between days 27 and 55. Arachidonic acid (ARA) was the major polyunsaturate in PL of the penguin's heart, where it formed about 20% (w/w) of FA at day 55. At the equivalent developmental stage, the heart PL of the chicken contained a 1.3-fold greater proportion of ARA, contained a fifth less DHA, and was almost devoid of EPA, whereas the latter FA was a significant component (7% of FA) of penguin heart PL. Similarly, in PL of leg and pectoral muscle, the chicken displayed about 1.4-fold more ARA, up to 50% less DHA, and far less EPA in comparison with the penguin. Thus, although ARA-rich PL profiles are achieved in the heart and muscle of the penguin embryo, these profiles are significantly affected by the high n-3 content of the yolk.

Animals↗
PubMed2002

Thyroid hormone deiodinases during embryonic development of the saltwater crocodile (Crocodylus porosus).

All tissues of the embryonic saltwater crocodile (Crocodylus porosus) gradually increased in weight during development except for lung tissue, which had a peak weight of 1.09 g at day 67, thereafter decreasing in weight. The brain was a relatively large organ. Deiodinase activities in liver, kidney, lung, heart, gut, and brain from day 29 to day 77 of development of the saltwater crocodile were investigated. High-K(m) reverse triiodothyronine (rT(3)) outer ring deiodination (ORD) activity was present in all tissues except the brain. Activity ranged from 559 +/- 51.3 pmol rT(3) deiodinated/mg protein/min in the liver at day 77 to below 10 pmol rT(3) deiodinated/mg protein/min in gut, lung, and heart tissue. rT(3) ORD increased during development in the liver and kidney but decreased in the gut and lung. Activity in the heart was very low (less than 2 pmol rT(3) deiodinated/mg protein/min) and did not change during development. Low-K(m) thyroxine (T(4)) ORD in liver and kidney tissue had peaks of activity around day 49 of incubation (0.52 and 0.09 fmol T(4) deiodinated/mg protein/min, respectively). After day 49, T(4) ORD activity in these tissues decreased. T(4) ORD activity in gut, lung, and heart was very low (less than 0.04 fmol T(4) deiodinated/mg protein/min), with activity in lung increasing slightly during the rest of development. T(4) ORD activity in the brain increased toward day 77 (0.14 +/- 0.03 fmol T(4) deiodinated/mg protein/min), illustrating its importance in local triiodothyronine (T(3)) production during brain development. T(3) inner ring deiodination activity was present only in the embryonic liver and peaked at day 49 (10.1 fmol T(3) deiodinated/mg protein/min), after which activity decreased.

Alligators and Crocodiles↗
PubMed2004

Dp1 is largely dispensable for embryonic development.

E2F/DP complexes activate or repress the transcription of E2F target genes, depending on the association of a pRB family member, thereby regulating cell cycle progression. Whereas the E2F family consists of seven members, the DP family contains only two (Dp1 and Dp2), Dp1 being the more highly expressed member. In contrast to the inactivation of individual E2F family members, we have recently demonstrated that loss of Dp1 results in embryonic lethality by embryonic day 12.5 (E12.5) due to the failure of extraembryonic lineages to develop and replicate DNA properly. To bypass this placental requirement and search for roles of Dp1 in the embryo proper, we generated Dp1-deficient embryonic stem (ES) cells that carry the ROSA26-LacZ marker and injected them into wild-type blastocysts to construct Dp1-deficient chimeras. Surprisingly, we recovered mid- to late gestational embryos (E12.5 to E17.5), in which the Dp1-deficient ES cells contributed strongly to most chimeric tissues as judged by X-Gal (5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside) staining and Western blotting. Importantly, the abundance of DP2 protein does not increase and the expression of an array of cell cycle genes is virtually unchanged in Dp1-deficient ES cells or chimeric E15.5 tissues with the absence of Dp1. Thus, Dp1 is largely dispensable for embryonic development, despite the absolute extraembryonic requirement for Dp1, which is highly reminiscent of the restricted roles for Rb and cyclins E1/E2 in vivo.

Animals↗
PubMed1999

The role of apoptosis in normal and abnormal embryonic development.

Programmed cell death or apoptosis is a widespread biological phenomenon. Apoptosis is characterized by typical cell features such as membrane blebbing, chromatin condensation, and DNA fragmentation. It involves a number of membrane receptors (e.g., Fas, TNFR) and a cascade of signal transduction steps resulting in the activation of a number of cysteine proteases known as caspases. Disordered apoptosis may lead to carcinogenesis and participates in the pathogenesis of Alzheimer disease, Parkinson disease, or AIDS. Programmed cell death plays an important role in the processes of gamete maturation as well as in embryo development, contributing to the appropriate formation of various organs and structures. Apoptosis is one of the mechanisms of action of various cytotoxic agents and teratogens. Teratogen-induced excessive death of embryonic cells is undoubtedly one of the most important events preceding the occurrence of structural abnormalities, regardless of their nature. Therefore understanding the mechanisms involved in physiological as well as in disturbed or dysregulated apoptosis may lead to the development of new methods of preventive treatment of various developmental abnormalities. The present review summarizes data on the mechanisms of programmed cell death and concentrates on apoptosis involved in normal or disturbed gametogenesis and in normal and abnormal embryonic development.

Apoptosis↗
PubMed1981

Preferential accumulation of [3H] corticosterone in chick brain during embryonic development.

In the present study, we examined the distribution of [3H]corticosterone ([3H]B) in chick embryonic brain during development using two different routes of administration: intracerebral and intraocular. After injection of 1 microCi into the brain of 8-day embryos, [3H]B was preferentially accumulated in the retinas, whereas regions such as cerebral hemispheres, optic tecta, and midbrain showed lower amounts of [3H]B. In 14-day embryos, a slightly higher amount of [3H]B was found in retinas and midbrain in comparison with other regions of the brain. After injection into the eye, [3H]B seemed to easily diffuse to brain regions and toe preferentially accumulate in the opposite eye and very slowly diffused to other brain areas. The accumulation of the hormone in the retina parallels the presence of hormone receptors reported by others. A correlation between the preferential accumulation of hormone and its action is proposed.

Animals↗