Theory in Biosciences最新文献

Recent results have shown that the human malaria-resistant hemoglobin S mutation originates de novo more frequently in the gene and in the population where it is of adaptive significance, namely, in the hemoglobin subunit beta gene compared to the nonresistant but otherwise identical 20A[Formula: see text]T mutation in the hemoglobin subunit delta gene, and in sub-Saharan Africans, who have been subject to intense malarial pressure for many generations, compared to northern Europeans, who have not. This finding raises a fundamental challenge to the traditional notion of accidental mutation. Here, we address this finding with the replacement hypothesis, according to which preexisting genetic interactions can lead directly and mechanistically to mutations that simplify and replace them. Thus, an evolutionary process under selection can gradually hone in on interactions of importance for the currently evolving adaptations, from which large-effect mutations follow that are relevant to these adaptations. We exemplify this hypothesis using multiple types of mutation, including gene fusion mutations, gene duplication mutations, A[Formula: see text]G mutations in RNA-edited sites and transcription-associated mutations, and place it in the broader context of a system-level view of mutation origination called interaction-based evolution. Potential consequences include that similarity of mutation pressures may contribute to parallel evolution in genetically related species, that the evolution of genome organization may be driven by mutational mechanisms, that transposable element movements may also be explained by replacement, and that long-term directed mutational responses to specific environmental pressures are possible. Such mutational phenomena need to be further tested by future studies in natural and artificial settings.

In animal species with separate sexes, abnormal individuals with a mix of phenotypically male and phenotypically female body parts are generally indicated as gynandromorphs, whereas individuals with intermediate sexual phenotypic traits are generally indicated as intersexes. However, this distinction, clear as it may seem, is neither universally agreed upon, nor free of critical issues. In consideration of the role of sex anomalies in understanding normal development, we reassess these phenomena of abnormal sexual development, taking into consideration the more recent advances in the study of sex determination and sexual differentiation. We argue that a distinction between gynandromorphism and intersexuality, although useful for descriptive purposes, is not always possible or sensible. We discuss the conceptual and terminological intricacies of the literature on this subject and provide reasons for largely, although not strictly, preferring a terminology based on descriptive rather than causal morphology, that is, on the observed phenotypic patterns rather on the causal process behind them.

There is an old attempt to divide the sciences into sciences of laws and the historical sciences. More recently, John Beatty has drawn the distinction so that biology is a historical science and urged that there are no genuinely biological laws. This paper shows that there are indeed biological laws, specifically statistical ones, notably in evolutionary theory. Moreover, all or almost all other areas of biology involve laws as well. Even history involves laws. Finally, the paper shows that this pervasiveness of laws is compatible with the most basic commitments of those who, like Beatty, would claim that biology is only historical.

The study of radiosensitivity and radioresistance of organisms exposed to ionizing radiation has acquired additional relevance since a new bio-concept, coined as The primacy of Proteome over Genome, was proposed and demonstrated elsewhere a few years ago. According to that finding, genome integrity would require an actively functioning Proteome. However, when exposure to radiation takes place, Reactive Oxygen Species (ROS) from water radiolysis induce protein carbonylation (PC), an irreversible oxidative Proteome damage. The bio-models used in that study were the radiosensitive Escherichia coli and the extraordinarily robust Deinococcus radiodurans. The production of ROS induces protective reactions rendering them non-reactive forms. Protective entities present in the cytosol, moieties smaller than 3 kDa, shield the Proteome against ROS, yielding protection against carbonylation. Shown in the present study is the fact that the fate of proteins functionality is determined by the magnitude of the Protein Carbonylation Yield (Y_PC), a quantity here analytically defined using published Y_PC numerical results. Analytical Y_PC expressions for E. coli and D. radiodurans were the input for a phenomenological approach, where the radiobiological magnitudes P_P and P_N, the probabilities for production of protein damage and ROS neutralization, respectively, were also analytically deduced. These highly relevant magnitudes, associated with key radiosensitivity and radioresistance issues, are addressed and discussed in this study. Among the plethora of information and conclusions derived from the present study, those endowed with higher conceptual degree, vis-à-vis the "Primacy of Proteome over Genome" concept, are as follows: (1) the ROS neutralization process in D. radiodurans reaches a maximum at a dose interval corresponding to the repairing shoulder. Therefore, it is a signature of the higher efficiency of the PC neutralization process. (2) ROS neutralization in D. radiodurans is nearly one order of magnitude higher than in E. coli, thus accounting for its extraordinary radioresistance. (3) Both physical (ROS-induced carbonyl radicals) and biological (protein modifications) processes are imbedded in the Protein Carbonylation Yield. The amalgamation of these two processes was accomplished by means of a statistical formalism.

The bio-cell cycle is controlled by a complex biochemical network of signaling pathways. Modeling such challenging networks accurately is imperative for the understanding of their detailed dynamical behavior. In this paper, we construct, analyze, and verify a hybrid Petri net (HPN) model of a complex biochemical network that captures the role of an important protein (namely p53) in deciding the fate of the cell. We model the behavior of the cell nucleus and cytoplasm as two stochastic and continuous Petri nets, respectively, combined together into a single HPN. We use simulative model checking to verify three different properties that capture the dynamical behavior of p53 protein with respect to the intensity of the ionizing radiation (IR) to which the cell is exposed. For each IR dose, 1000 simulation runs are carried out to verify each property. Our verification results showed that the fluctuations in p53, which relies on IR intensity, are compatible with the findings of the preceding simulation studies that have previously examined the role of p53 in cell fate decision.

The aim of this study was an analytical justification of the emergence and presence of the phenomenon of war among hominins, taking into account males' genetic benefits gained through war in the natural environment. Based on chimpanzee behavior, the analytical model of the primary warrior balance was explored, comparing the risk of a war expedition with the genetic profits from war rape-"life and death balance". On the profits side, genetic gains possible to obtain in terms of permanent attractiveness of females (warrior status and abductions of females) were also included. Kin cooperation, parochial altruism, and "partisan strategy" have been defined as psychological mechanisms that enable effective group violence. Male genetic benefit from a war rape could exceed the risk of a warrior's death in the chimpanzee-human LCA species; transition from the herd to the patriarchal tribal social system could increase warrior's genetic gains from war. At the root of war lie sexual limitations of cooperating males, induced by female sexual preferences and lack of the permanent female sexual drive. War rape allows reproductive success for dominated and thus sexually restricted males. Tendencies for group aggression to gain access to out-group females (the war gene) are common among sexually restricted men. Resource-rich areas favor increase in human population density, this affects group territoriality and promotes intergroup conflicts, and thus patriarchy. Roots of conventional patriarchal marriage are strongly combined with war-"the right to land entails the right to a female".

Chilli leaf curl Ahmedabad virus (ChiLCAV), a begomovirus belonging to the family Geminiviridae, has been reported for its occurrence in India, infecting chilli and tomato plants. The viral proteins associated with ChiLCAV involves in the primary pathogenesis and transmission of the virus by whitefly. Viral protein interactions with host proteins show the dynamics of structural binding and interaction in their infection cycle. At the same time, plants have multiple defence mechanisms against bacterial and viral infections. Secondary metabolites play a significant role in the inborne defence mechanism of plants. Host proteins are also the prime producers of secondary metabolites. In the present study, we evaluated the host protein SnRK1 interaction with all six viral proteins (V1, V2, C1, C2, C3 and C4). Apart from C4, all the other viral proteins showed appreciable binding and interaction with SnRK1. SnRK1 has the regulation mechanism for the accumulation of diterpenoids, secondary metabolites. Flavonoids are secondary metabolites produced by the plant under stress conditions. Further, we studied the binding and interaction of six selected flavonoids produced by Solanaceae family members with all the ChiLCAV proteins. All six selected flavonoids showed considerable binding energy with all viral proteins. Each flavonoid showed high binding energy with different viral proteins. Molecular docking is carried out for both flavonoids and the host protein SnRK1. These in silico interactions and docking studies could be useful for understanding the plants defence mechanism against viral infections at the molecular level.

The origin of life was a cosmic event happened on primitive Earth. A critical problem to better understand the origins of life in Earth is the search for chemical scenarios on which the basic building blocks of biological molecules could be produced. Classic works in pre-biotic chemistry frequently considered early Earth as an homogeneous atmosphere constituted by chemical elements such as methane (CH₄), ammonia (NH₃), water (H₂O), hydrogen (H₂) and hydrogen sulfide (H₂S). Under that scenario, Stanley Miller was capable to produce amino acids and solved the question about the abiotic origin of proteins. Conversely, the origin of nucleic acids has tricked scientists for decades once nucleotides are complex, though necessary molecules to allow the existence of life. Here we review possible chemical scenarios that allowed not only the formation of nucleotides but also other significant biomolecules. We aim to provide a theoretical solution for the origin of biomolecules at specific sites named "Prebiotic Chemical Refugia." Prebiotic chemical refugium should therefore be understood as a geographic site in prebiotic Earth on which certain chemical elements were accumulated in higher proportion than expected, facilitating the production of basic building blocks for biomolecules. This higher proportion should not be understood as static, but dynamic; once the physicochemical conditions of our planet changed periodically. These different concentration of elements, together with geochemical and astronomical changes along days, synodic months and years provided somewhat periodic changes in temperature, pressure, electromagnetic fields, and conditions of humidity, among other features. Recent and classic works suggesting most likely prebiotic refugia on which the main building blocks for biological molecules might be accumulated are reviewed and discussed.

In this paper, a new mathematical model that describes the dynamics of the within-host COVID-19 epidemic is formulated. We show the stochastic dynamics of Target-Latent-Infected-Virus free within the human body with discrete delay and noise. Positivity and uniqueness of the solutions are established. Our study shows the extinction and persistence of the disease inside the human body through the stability analysis of the disease-free equilibrium [Formula: see text] and the endemic equilibrium [Formula: see text], respectively. Moreover, we show the impact of delay tactics and noise on the extinction of the disease. The most interesting result is even if the deterministic system is inevitably pandemic at a specific point, extinction will become possible in the stochastic version of our model.

We study seasonal mutualistic interactions between two species. The model takes into account the climate-mediated shifts that can change the phenologies of mutualistic species. We show conditions on the parameters of the model that guarantee global stability. Numerical simulations are performed for different scenarios associated with seasonal changes. They show that if periodic time-dependence is used to approximate an almost periodic one, then not only the densities of the mutualistic populations but also the overlapping intervals describing the interval of co-occurrence can be either underestimated or overestimated. Therefore, using an almost periodic model can be more adequate to design conservation strategies for asynchronous phenology.