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At least 1,027 records · Page 57Linked to original sources
PubMed1984

The present state in the phylogeny and ontogeny of hormone receptors.

Presence of signal receivers (for food, toxic, substances, "hostile" cells etc.) is essential at all levels of phylogenesis. The first encounter of a "hormone to be" with an aspecific membrane structure ("receptor to be") could result in the formation of a lasting receptor-hormone connection if it is adventageous for the cell or organism (which contains the cell), during phylogeny. At higher levels of phylogenesis receptors (ontogenetically) develop according to the differentiation program of the cell, however reinforcement (by the hormone) is necessary in a critical (neonatal) period of receptor development. This is the hormonal imprinting. In that time the receptor could be damaged by the presence of molecules analogous to the hormone. The hormonal imprinting belongs to the perinatal recognition mechanisms of organisms. The possible mechanisms of receptor development are also discussed.

Aging↗
PubMed1976

Neuronal circuits involved in learning: the use of modifiable synapses in the simulation of behavior.

Our present knowledge of brain structure and function requires that any model of neuronal circuitry designed to account for learning must satisfy three conditions. It must (1) meet economy restrictions on the number of cells in the brain, (2) use the same set of cells to account for a number of different behaviors, and (3) not require a detailed embryological specification of its connections. Previously published models have failed to meet one or more of these conditions. In this paper, a model is presented which does satisfy them, and in doing so accounts in detail for classical conditioning, operant conditioning, and other learning tasks. The model employs the types of synapses proposed by Burke and Hebb in simple modular circuits as a means of providing independent storage of information at each modifiable synapse.

Animals↗
PubMedDate not supplied

[Does DNA alone determine the development of the organism? (the information aspect of the problem)].

Two closely related controversial problems are discussed: whether the developmental processes can be reduced to the synthesis of polypeptides encoded in DNA, and whether the information in DNA is equivalent to that in the adult organism. Critically considered are the ideas that DNA is only responsible for the protein synthesis, whereas morphogenesis proceeds independently and according to epigenetic regularities of its own. It is stated that development is the realization of genetic information in which more elementary (molecular) processes unambiguously determine a more complex cellular level which in its turn determines morphogenesis of tissues and organs. Various mechanisms of the appearance of new information in the course of development are considered. The statement is made that new information concerns only some individual characters of the organism, whereas most of information that determines the process of development and the structure of the adult organism is created in the course of evolution, is stored in DNA and inherited.

Animals↗
PubMedDate not supplied

Molecular evolution: first enzymes, gases as substrates and genetic templates.

A fundamental problem in biology is the self-assembly of the first cells capable of growth and division under anoxic conditions on the Earth. Evolution proceeded by self-assembling and self-replicating cells that reproduced their own genetic information and also changed their genetic code over time. Was it also possible that some of the first proteins were catalytic and used gases as substrates and also acted as genetic templates? This paper explores the possibility that primitive protein enzymes used gases as their substrates, and reverse translation may have been a feature in the self-assembly of the first cell(s).

Cells↗
PubMed1989

Selection of new biological activities from random nucleotide sequences: evolutionary and practical considerations.

Recent advances in the selection of biologically active DNA sequences from random populations are reviewed. Within the framework of evolution, forces are considered that have precluded the testing of all possible DNA sequences, purely with regard to their functionality as genetic regulatory elements or protein coding sequences. Examples are drawn from cassette mutagenesis of enzyme active sites, protein domain replacement by fusion with random genomic digests, and the selection of bacterial promoters from random DNA. Efforts to derive new activities are examined, and the likelihood of future success is evaluated.

Base Sequence↗
PubMed1985

Cross-species gene transfer; implications for a new theory of evolution.

It has been established that genes can be transferred and expressed among procaryotes of different species. I am hypothesizing--and there is mounting evidence for this conclusion--that genes are transferred and expressed among all species, and that such exchange is facilitated by, and can help account for, the existence of the biological unities, from the uniform genetic code to the cross-species similarity of the stages of embryological development. If this idea is correct, the uniformity of the genetic code would allow organisms to decipher and use genes transposed from chromosomes of foreign species, and the shared sequence of embryological development within each phylum would allow the organism to integrate these genes, particularly when the genes affect complex morphological traits. The cross-species gene transfer model could help explain many observations which have puzzled evolutionists, such as rapid bursts in evolution and the widespread occurrence of parallelism in the fossil record.

Animals↗
PubMed2006

Longevity and the evolution of the mitochondrial DNA-coded proteins in mammals.

The amino acids sequences of the mitochondrial DNA-coded peptides of placental mammals evolved at different rates in different branches of the mammalian phylogenetic tree. Adaptive selection was suggested to account for the faster evolution of some mitochondrial DNA-coded proteins in several branches of the mammalian tree, but the driving force(s) for the accelerated evolution has not been elucidated. Mitochondria generate reactive oxygen species (ROS) that appear to constrain the life span of many species. Therefore, I tested the hypothesis that the evolution of mammalian longevity drives the accelerated evolution of mitochondrial DNA-coded peptides. Using rodents as an outgroup for a clad that included most placental mammals (excluding rodents and hedgehogs) the computed rates of amino acid substitution per site were positively correlated with genus longevity (maximal observed averaged life span) for most of the mitochondrial DNA-coded peptides. The substitution per site of ATP6, the proton conducting subunit of ATPsynthase, CYTB, the core subunit of ubiquinone oxidoreductase that participate in both electron and proton transport, and ND3, a subunit of NADH dehydrogenase, showed the strongest correlations with longevity. Additional confirmation for the hypothesis was obtained by the observation that the genetic distances between placental mammals species that belong to different orders are positively correlated with the sum of longevities of the species pairs. The substitutions per site for the entire amino acid sequence coded by the heavy strand mtDNA were also positively correlated with the average longevities of the placental mammals orders. These results support the hypothesis that the evolution of longevity in mammals drove the accelerated evolution of mtDNA-coded peptide. It is suggested that, in mammals, adaptive selection of mutations that decrease the rate of production of reactive oxygen species, directly or indirectly (e.g. by increasing proton leak), increases longevity.

Animals↗
PubMedDate not supplied

Evolution within the multigene family coding for the class I histocompatibility antigens: the case of the mouse t-haplotypes.

The t-haplotypes of the house mouse are defined by several genetic events which involve about one-third of chromosome 17 and include the major histocompatibility complex (MHC). One of the primary features of complete t-haplotypes is the nearly complete suppression of recombination between a t-chromosome and a wild-type chromosome 17. If we assume that all genetic exchanges are abolished because of the inhibition of recombination, the class I genes of the MHC can be used as vicinity markers of t-haplotypes. We have studied the H-2K, D and L genes of 10 independant t-haplotypes and have found that their H-2K genes are rather polymorphic, although always very similar or identical to H-2K genes of laboratory mice. By contrast, the DL-Tla region is nearly constant. It is suggested that the t-haplotypes reveal the existence of several mechanisms involved in the evolution of the MHC, one of which is possibly the greater "mobility" of H-2K genes in the genome.

Animals↗