scholarly journals The origin of the central dogma through conflicting multilevel selection

2019 ◽  
Author(s):  
Nobuto Takeuchi ◽  
Kunihiko Kaneko

AbstractThe central dogma of molecular biology rests on two kinds of asymmetry between genomes and enzymes: informatic asymmetry, where information flows from genomes to enzymes but not from enzymes to genomes; and catalytic asymmetry, where enzymes provide chemical catalysis but genomes do not. How did these asymmetries originate? Here we show that these asymmetries can spontaneously arise from conflict between selection at the molecular level and selection at the cellular level. We developed a model consisting of a population of protocells, each containing a population of replicating catalytic molecules. The molecules are assumed to face a trade-off between serving as catalysts and serving as templates. This trade-off causes conflicting multilevel selection: serving as catalysts is favoured by selection between protocells, whereas serving as templates is favoured by selection between molecules within protocells. This conflict induces informatic and catalytic symmetry breaking, whereby the molecules differentiate into genomes and enzymes, establishing the central dogma. We show mathematically that the symmetry breaking is caused by a positive feedback between Fisher’s reproductive values and the relative impact of selection at different levels. This feedback induces a division of labour between genomes and enzymes, provided variation at the molecular level is sufficiently large relative to variation at the cellular level, a condition that is expected to hinder the evolution of altruism. Taken together, our results suggest that the central dogma is a logical consequence of conflicting multilevel selection.

2019 ◽  
Vol 286 (1912) ◽  
pp. 20191359 ◽  
Author(s):  
Nobuto Takeuchi ◽  
Kunihiko Kaneko

The central dogma of molecular biology rests on two kinds of asymmetry between genomes and enzymes: informatic asymmetry, where information flows from genomes to enzymes but not from enzymes to genomes; and catalytic asymmetry, where enzymes provide chemical catalysis but genomes do not. How did these asymmetries originate? Here, we show that these asymmetries can spontaneously arise from conflict between selection at the molecular level and selection at the cellular level. We developed a model consisting of a population of protocells, each containing a population of replicating catalytic molecules. The molecules are assumed to face a trade-off between serving as catalysts and serving as templates. This trade-off causes conflicting multilevel selection: serving as catalysts is favoured by selection between protocells, whereas serving as templates is favoured by selection between molecules within protocells. This conflict induces informatic and catalytic symmetry breaking, whereby the molecules differentiate into genomes and enzymes, establishing the central dogma. We show mathematically that the symmetry breaking is caused by a positive feedback between Fisher’s reproductive values and the relative impact of selection at different levels. This feedback induces a division of labour between genomes and enzymes, provided variation at the molecular level is sufficiently large relative to variation at the cellular level, a condition that is expected to hinder the evolution of altruism. Taken together, our results suggest that the central dogma is a logical consequence of conflicting multilevel selection.


Author(s):  
Tian Wu ◽  
Danyan Hu ◽  
Qingfen Wang

Abstract Background Noni (Morinda citrifolia Linn.) is a tropical tree that bears climacteric fruit. Previous observations and research have shown that the second day (2 d) after harvest is the most important demarcation point when the fruit has the same appearance as the freshly picked fruit (0 d); however, they are beginning to become water spot appearance. We performed a conjoint analysis of metabolome and transcriptome data for noni fruit of 0 d and 2 d to reveal what happened to the fruit at the molecular level. Genes and metabolites were annotated to KEGG pathways and the co-annotated KEGG pathways were used as a statistical analysis. Results We found 25 pathways that were significantly altered at both metabolic and transcriptional levels, including a total of 285 differentially expressed genes (DEGs) and 11 differential metabolites through an integrative analysis of transcriptomics and metabolomics. The energy metabolism and pathways originating from phenylalanine were disturbed the most. The upregulated resistance metabolites and genes implied the increase of resistance and energy consumption in the postharvest noni fruit. Most genes involved in glycolysis were downregulated, further limiting the available energy. This lack of energy led noni fruit to water spot appearance, a prelude to softening. The metabolites and genes related to the resistance and energy interacted and restricted each other to keep noni fruit seemingly hard within two days after harvest, but actually the softening was already unstoppable. Conclusions This study provides a new insight into the relationship between the metabolites and genes of noni fruit, as well as a foundation for further clarification of the post-ripening mechanism in noni fruit.


1956 ◽  
Vol 34 (1) ◽  
pp. 25-38
Author(s):  
J. Gordin Kaplan ◽  
Woon-Ki Paik

The rate with which n-butanol alters the properties of yeast catalase has been studied as a function of temperature and concentration of altering agent. Activation energies for catalase alteration lay within the rather narrow range of 20–23 kcal./mole, thus confirming a prediction made previously on the basis of the difference in energies of activation for heat destruction of altered and unaltered catalases. Alteration by optimal concentration of butanol was a reaction of zero order. Chloroform also altered yeast catalase with an activation energy within this range of μ values. The close agreement in μ values leads us to conclude that the action of these two altering agents, at all concentrations, is characterized by the same rate-limiting step, even though their action differs in other respects. It was concluded that catalase alteration is probably all-or-none on the molecular level, rather than on the cellular level. Alteration was invariably accompanied by a decrease in the size of the treated cells; alteration was sometimes accompanied by changes in the cytochrome spectrum, but there was no causal connection between these two events. These data are consistent with the interfacial hypothesis, which, in its present crude form, pictures alteration as consisting essentially in the desorption of catalase from some intracellular interface at which it is normally bound in the intact cell.


2003 ◽  
Vol 26 (1) ◽  
pp. 84-85
Author(s):  
Hendrik Pieter Barendregt

AbstractThe target article presents a model for schizophrenia extending four levels of abstraction: molecules, cells, cognition, and syndrome. An important notion in the model is that of coordination, applicable to both the level of cells and of cognition. The molecular level provides an “implementation” of the coordination at the cellular level, which in turn underlies the coordination at the cognitive level, giving rise to the clinical symptoms.


Author(s):  
Irene Man ◽  
Simopekka Vänskä ◽  
Matti Lehtinen ◽  
Johannes A Bogaards

Abstract Background Although human papillomavirus (HPV) vaccines are highly efficacious in protecting against HPV infections and related diseases, vaccination may trigger replacement by nontargeted genotypes if these compete with the vaccine-targeted types. HPV genotype replacement has been deemed unlikely, based on the lack of systematic increases in the prevalence of nonvaccine-type (NVT) infection in the first decade after vaccination, and on the presence of cross-protection for some NVTs. Methods To investigate whether type replacement can be inferred from early postvaccination surveillance, we constructed a transmission model in which a vaccine type and an NVT compete through infection-induced cross-immunity. We simulated scenarios of different levels of cross-immunity and vaccine-induced cross-protection to the NVT. We validated whether commonly used measures correctly indicate type replacement in the long run. Results Type replacement is a trade-off between cross-immunity and cross-protection; cross-immunity leads to type replacement unless cross-protection is strong enough. With weak cross-protection, NVT prevalence may initially decrease before rebounding into type replacement, exhibiting a honeymoon period. Importantly, vaccine effectiveness for NVTs is inadequate for indicating type replacement. Conclusions Although postvaccination surveillance thus far is reassuring, it is still too early to preclude type replacement. Monitoring of NVTs remains pivotal in gauging population-level impacts of HPV vaccination.


Author(s):  
Anna Filipiak ◽  
Tadeusz Malewski ◽  
Ewa Matczyńska ◽  
Marek Tomalak

Abstract Bursaphelenchus xylophilus is an emerging pathogenic nematode that is responsible for a devastating epidemic of pine wilt disease worldwide, causing severe ecological damage and economic losses to forestry. Two forms of this nematode have been reported, i.e., with strong and weak virulence, commonly referred as virulent and avirulent strains. However, the pathogenicity-related genes of B. xylophilus are not sufficiently characterized. In this study, to find pathogenesis related genes we re-sequenced and compared genomes of two virulent and two avirulent populations. We identified genes affected by genomic variation, and functional annotation of those genes indicated that some of them might play potential roles in pathogenesis. The performed analysis showed that both avirulent populations differed from the virulent ones by 1576 genes with high impact variants. Demonstration of genetic differences between virulent and avirulent strains will provide effective methods to distinguish these two nematode virulence forms at the molecular level. The reported results provide basic information that can facilitate development of a better diagnosis for B. xylophilus isolates/strains which present different levels of virulence and better understanding of the molecular mechanism involved in the development of the PWD.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Tuqyah Abdullah Al Qazlan ◽  
Aboubekeur Hamdi-Cherif ◽  
Chafia Kara-Mohamed

To address one of the most challenging issues at the cellular level, this paper surveys the fuzzy methods used in gene regulatory networks (GRNs) inference. GRNs represent causal relationships between genes that have a direct influence, trough protein production, on the life and the development of living organisms and provide a useful contribution to the understanding of the cellular functions as well as the mechanisms of diseases. Fuzzy systems are based on handling imprecise knowledge, such as biological information. They provide viable computational tools for inferring GRNs from gene expression data, thus contributing to the discovery of gene interactions responsible for specific diseases and/orad hoccorrecting therapies. Increasing computational power and high throughput technologies have provided powerful means to manage these challenging digital ecosystems at different levels from cell to society globally. The main aim of this paper is to report, present, and discuss the main contributions of this multidisciplinary field in a coherent and structured framework.


2005 ◽  
Vol 152 (1) ◽  
pp. 11-31 ◽  
Author(s):  
Primus E Mullis

The application of the powerful tool molecular biology has made it possible to ask questions not only about hormone production and action but also to characterize many of the receptor molecules that initiate responses to the hormones. We are beginning to understand how cells may regulate the expression of genes and how hormones intervene in regulatory processes to adjust the expression of individual genes. In addition, great strides have been made in understanding how individual cells talk to each other through locally released factors to coordinate growth, differentiation, secretion, and other responses within a tissue. In this review I (1) focus on developmental aspects of the pituitary gland, (2) focus on the different components of the growth hormone axis and (3) examine the different altered genes and their related growth factors and/or regulatory systems that play an important physiological and pathophysiological role in growth. Further, as we have already entered the ‘post-genomic’ area, in which not only a defect at the molecular level becomes important but also its functional impact at the cellular level, I concentrate in the last part on some of the most important aspects of cell biology and secretion.


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