Effects of vitamin A and other retinoids on the differentiation and morphogenesis of the integument and limbs of vertebrates

1991 ◽  
Vol 69 (2) ◽  
pp. 263-273 ◽  
Author(s):  
Keith J. Johnson ◽  
Steven R. Scadding
Keyword(s):  
Cell Differentiation ◽  
Vitamin A ◽  
Thyroid Hormones ◽  
Mechanism Of Action ◽  
Limb Development ◽  
Common Mechanism ◽  
Complex Processes ◽  
Normal Differentiation ◽  
Pattern Regulation ◽  
Related Compounds

Exogenous vitamin A is a well-known teratogen and modifies the course of cell differentiation, embryonic development, and morphogenesis. Recent evidence has shown that vitamin A and related compounds (the "retinoids") are likely natural morphogens, carrying out important roles in such processes as limb development and epithelial differentiation. Retinoids can modify the differentiation of individual cells and can induce specific modifications of morphogenesis in such structures as epithelial appendages, developing limbs, and regenerating limbs. Evidence is accumulating that there may be a common mechanism of action underlying these diverse phenomena. Retinoids may enter cells and induce changes in gene transcription in a manner similar to that reported for steroid and thyroid hormones and their receptors. Retinoids are particularly useful probes in the study of cell differentiation and morphogenesis because an understanding of their action can provide clues to the mechanisms involved in the complex processes of normal differentiation, morphogenesis, and pattern regulation.

Comparison of the effects of vitamin A on limb development and regeneration in Xenopus laevis tadpoles

Development ◽  
1986 ◽  
Vol 91 (1) ◽  
pp. 35-53
Author(s):  
S. R. Scadding ◽  
M. Maden
Keyword(s):  
Cell Cycle ◽  
Vitamin A ◽  
Xenopus Laevis ◽  
Limb Development ◽  
Complete Inhibition ◽  
Complete Suppression ◽  
Dual Action ◽  
Pattern Regulation

The purpose of these experiments was to compare the effects of vitamin A on developing and regenerating limbs in Xenopus laevis tadpoles. Each tadpole had one hindlimb amputated to induce regeneration while the contralateral developing limb was left intact. Tadpoles at stages 50 through 54 were treated by immersion in retinol palmitate at doses ranging from 0·3 to 75 i.u.ml−1, for periods ranging from 1 to 14 days. Developing limbs usually became hypomorphic as a result of the treatment, with results varying with stage and treatment from slight phalange derangements to total disruption of pattern, or complete inhibition of limb development. Regenerating limbs gave a variety of responses including hypomorphic regeneration, proximodistal or anteroposterior duplication of skeletal elements, or complete suppression of regeneration. The response to retinol palmitate of developing limbs was clearly different from regenerating limbs. Hypotheses which might explain the results were discussed and a hypothesis which, proposed a dual action of vitamin A affecting both the cell cycle and the mechanism of pattern regulation was proposed.

scholarly journals Bacteriophage-derived CHAP domain protein, P128, kills Staphylococcus cells by cleaving interpeptide cross-bridge of peptidoglycan

Microbiology ◽  
2014 ◽  
Vol 160 (10) ◽  
pp. 2157-2169 ◽  
Author(s):  
Sudarson Sundarrajan ◽  
Junjappa Raghupatil ◽  
Aradhana Vipra ◽  
Nagalakshmi Narasimhaswamy ◽  
Sanjeev Saravanan ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mechanism Of Action ◽  
Catalytic Domain ◽  
Antibiotic Sensitivity ◽  
High Sensitivity ◽  
Common Mechanism ◽  
Cross Bridge ◽  
Sensitivity Pattern

P128 is an anti-staphylococcal protein consisting of the Staphylococcus aureus phage-K-derived tail-associated muralytic enzyme (TAME) catalytic domain (Lys16) fused with the cell-wall-binding SH3b domain of lysostaphin. In order to understand the mechanism of action and emergence of resistance to P128, we isolated mutants of Staphylococcus spp., including meticillin-resistant Staphylococcus aureus (MRSA), resistant to P128. In addition to P128, the mutants also showed resistance to Lys16, the catalytic domain of P128. The mutants showed loss of fitness as shown by reduced rate of growth in vitro. One of the mutants tested was found to show reduced virulence in animal models of S. aureus septicaemia suggesting loss of fitness in vivo as well. Analysis of the antibiotic sensitivity pattern showed that the mutants derived from MRSA strains had become sensitive to meticillin and other β-lactams. Interestingly, the mutant cells were resistant to the lytic action of phage K, although the phage was able to adsorb to these cells. Sequencing of the femA gene of three P128-resistant mutants showed either a truncation or deletion in femA, suggesting that improper cross-bridge formation in S. aureus could be causing resistance to P128. Using glutathione S-transferase (GST) fusion peptides as substrates it was found that both P128 and Lys16 were capable of cleaving a pentaglycine sequence, suggesting that P128 might be killing S. aureus by cleaving the pentaglycine cross-bridge of peptidoglycan. Moreover, peptides corresponding to the reported cross-bridge of Staphylococcus haemolyticus (GGSGG, AGSGG), which were not cleaved by lysostaphin, were cleaved efficiently by P128. This was also reflected in high sensitivity of S. haemolyticus to P128. This showed that in spite of sharing a common mechanism of action with lysostaphin, P128 has unique properties, which allow it to act on certain lysostaphin-resistant Staphylococcus strains.

Furoxan-, alkylnitrate-derivatives and related compounds as anti-trypanosomatid agents: Mechanism of action studies

2008 ◽  
Vol 16 (17) ◽  
pp. 7900-7907 ◽  
Author(s):  
Lucı´a Boiani ◽  
Gabriela Aguirre ◽  
Mercedes González ◽  
Hugo Cerecetto ◽  
Agustina Chidichimo ◽  
...  
Keyword(s):  
Mechanism Of Action ◽  
Related Compounds
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