Plasticity comparisons between plants and animals: Concepts and mechanisms

This review attempts to present an integrated update of the issue of comparisons of phenotypic plasticity between plants and animals by presenting the problem and its integrated solutions via a whole-organism perspective within an evolutionary framework. Plants and animals differ in two important aspects: mobility and longevity. These features can have important implications for plasticity, and plasticity may even have facilitated greater longevity in plants. Furthermore, somatic genetic mosaicism, intra-organismal selection, and genomic instability contribute to the maintenance of an adaptive phenotype that is especially relevant to long-lived plants. It is contended that a cross-kingdom phylogenetic examination of sensors, messengers and responses that constitute the plasticity repertoire would be more useful than dichotomizing the plant and animal kingdoms. Furthermore, physicochemical factors must be viewed cohesively in the signal reception and transduction pathways leading to plastic responses. Comparison of unitary versus modular organisms could also provide useful insights into the range of expected plastic responses. An integrated approach that combines evolutionary theory and evolutionary history with signal-response mechanisms will yield the most insights into phenotypic plasticity in all its forms.Key words: electrical signaling, genomic instability, mechanotransduction, phenotypic plasticity, plant volatiles, reactive oxygen species, ROS signaling     

Obesity and cancer: pathophysiological and biological mechanisms

Excess body weight (overweight and obesity) is characterized by chronic hyperinsulinaemia and insulin resistance, and is implicated both in cancer risk and cancer mortality. The list of cancers at increased risk of development in an "obesogenic" environment include common adult cancers such as endometrium, post-menopausal breast, colon and kidney, but also less common malignancies such as leukaemia, multiple myeloma, and non-Hodgkin's lymphoma. The pathophysiological and biological mechanisms underpinning these associations are only starting to be understood. Insulin resistance is at the heart of many, but there are several other candidate systems including insulin-like growth factors, sex steroids, adipokines, obesity-related inflammatory markers, the nuclear factor kappa beta (NF-kappa B) system and oxidative stresses. With such as diversity of obesity-related cancers, it is unlikely that there is a "one system fits all" mechanism. While public health strategies to curb the spread of the obesity epidemic appear ineffective, there is a need to better understand the processes linking obesity and cancer as a pre-requisite to the development of new approaches to the prevention and treatment of obesity-related cancers.     

Aspirin and cancer: biological mechanisms and clinical outcomes

Evidence on aspirin and cancer comes from two main sources: (1) the effect of aspirin upon biological mechanisms in cancer, and (2) clinical studies of patients with cancer, some of whom take aspirin. A series of systematic literature searches identified published reports relevant to these two sources. The effects of aspirin upon biological mechanisms involved in cancer initiation and growth appear to generate reasonable expectations of effects upon the progress and mortality of cancer. Clinical evidence on aspirin appears overall to be favourable to the use of aspirin, but evidence from randomized trials is limited, and inconsistent. The main body of evidence comes from meta-analyses of observational studies of patients with a wide range of cancers, about 25% of whom were taking aspirin. Heterogeneity is large but, overall, aspirin is associated with increases in survival and reductions in metastatic spread and vascular complications of different cancers. It is important that evaluations of aspirin used as an adjunct cancer treatment are based upon all the available relevant evidence, and there appears to be a marked harmony between the effects of aspirin upon biological mechanisms and upon the clinical progress of cancer.     

Various biological effects of solar radiation on skin and their mechanisms: implications for phototherapy

ABSTRACT

The skin protects our body from various external factors, such as chemical and physical stimuli, microorganisms, and sunlight. Sunlight is a representative environmental factor that considerably influences the physiological activity of our bodies. The molecular mechanisms and detrimental effects of ultraviolet rays (UVR) on skin have been thoroughly investigated. Chronic exposure to UVR generally causes skin damage and eventually induces wrinkle formation and reduced elasticity of the skin. Several studies have shown that infrared rays (IR) also lead to the breakdown of collagen fibers in the skin. However, several reports have demonstrated that the appropriate use of UVR or IR can have beneficial effects on skin-related diseases. Additionally, it has been revealed that visible light of different wavelengths has various biological effects on the skin. Interestingly, several recent studies have reported that photoreceptors are also expressed in the skin, similar to those in the eyes.

Based on these data, I discuss the various physiological effects of sunlight on the skin and provide insights on the use of phototherapy, which uses a specific wavelength of sunlight as a non-invasive method, to improve skin-related disorders.     

Long-term effects of ionising radiation on the brain: cause for concern?

There is no clear evidence proving or disproving that ionising radiation is causally linked with neurodegenerative diseases such as Parkinson’s and Alzheimer’s. However, it is known that high doses of ionising radiation to the head (20–50 Gy) lead to severe learning and memory impairment which is characteristical for Alzheimer’s. The cumulative doses of ionising radiation to the Western population are accruing, mostly due to the explosive growth of medical imaging procedures. Children are in particular prone to ionising radiation as the molecular processes within the brain are not completely finished. Furthermore, they have a long lifespan under risk. We wish to open a debate if such low doses of radiation exposure may lead to delayed long-term cognitive and other defects, albeit at a lower frequency than those observed during application of high doses. Further, we want to sensitise the society towards the risks of ionising radiation. To achieve these aims, we will recapitulate the known symptoms of Parkinson’s and Alzheimer’s on the molecular level and incorporate data of mainly low- and moderate-ionising radiation (<5 Gy). Thus, we want to highlight in general the potential similarities of both the neurodegenerative and radiation-induced pathways. We will propose a mechanistic model for radiation-induced neurodegeneration pointing out mitochondria as a key element. This includes effects of oxidative stress and neuroinflammation—all fundamental players of neurodegenerative diseases.     

Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation

ABSTRACT

This review aims to cover experimental data on oxidative effects of low-intensity radiofrequency radiation (RFR) in living cells. Analysis of the currently available peer-reviewed scientific literature reveals molecular effects induced by low-intensity RFR in living cells; this includes significant activation of key pathways generating reactive oxygen species (ROS), activation of peroxidation, oxidative damage of DNA and changes in the activity of antioxidant enzymes. It indicates that among 100 currently available peer-reviewed studies dealing with oxidative effects of low-intensity RFR, in general, 93 confirmed that RFR induces oxidative effects in biological systems. A wide pathogenic potential of the induced ROS and their involvement in cell signaling pathways explains a range of biological/health effects of low-intensity RFR, which include both cancer and non-cancer pathologies. In conclusion, our analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.     

Individual response of humans to ionising radiation: governing factors and importance for radiological protection

Tissue reactions and stochastic effects after exposure to ionising radiation are variable between individuals but the factors and mechanisms governing individual responses are not well understood. Individual responses can be measured at different levels of biological organization and using different endpoints following varying doses of radiation, including: cancers, non-cancer diseases and mortality in the whole organism; normal tissue reactions after exposures; and, cellular endpoints such as chromosomal damage and molecular alterations. There is no doubt that many factors influence the responses of people to radiation to different degrees. In addition to the obvious general factors of radiation quality, dose, dose rate and the tissue (sub)volume irradiated, recognized and potential determining factors include age, sex, life style (e.g., smoking, diet, possibly body mass index), environmental factors, genetics and epigenetics, stochastic distribution of cellular events, and systemic comorbidities such as diabetes or viral infections. Genetic factors are commonly thought to be a substantial contributor to individual response to radiation. Apart from a small number of rare monogenic diseases such as ataxia telangiectasia, the inheritance of an abnormally responsive phenotype among a population of healthy individuals does not follow a classical Mendelian inheritance pattern. Rather it is considered to be a multi-factorial, complex trait.     

Haplotype diversity: the link between statistical and biological association

In the rapidly growing field of association mapping in plants, the use of (marker) haplotypes rather than single markers can be an effective way of improving detection power. Here, we highlight the information that can be obtained from deducing the historical relationships between haplotypes. The ordering of haplotype classes according to deduced historical relationships should further enhance association detection power, but can also be used to predict the genotypic and phenotypic values of unobserved germplasm.     

Non-targeted effects of ionising radiation—Implications for low dose risk

Non-DNA targeted effects of ionising radiation, which include genomic instability, and a variety of bystander effects including abscopal effects and bystander mediated adaptive response, have raised concerns about the magnitude of low-dose radiation risk. Genomic instability, bystander effects and adaptive responses are powered by fundamental, but not clearly understood systems that maintain tissue homeostasis. Despite excellent research in this field by various groups, there are still gaps in our understanding of the likely mechanisms associated with non-DNA targeted effects, particularly with respect to systemic (human health) consequences at low and intermediate doses of ionising radiation. Other outstanding questions include links between the different non-targeted responses and the variations in response observed between individuals and cell lines, possibly a function of genetic background. Furthermore, it is still not known what the initial target and early interactions in cells are that give rise to non-targeted responses in neighbouring or descendant cells. This paper provides a commentary on the current state of the field as a result of the non-targeted effects of ionising radiation (NOTE) Integrated Project funded by the European Union. Here we critically examine the evidence for non-targeted effects, discuss apparently contradictory results and consider implications for low-dose radiation health effects.     

Dose limits for occupational exposure to ionising radiation and genotoxic carcinogens: a German perspective

This paper summarises the view of the German Commission on Radiological Protection (“Strahlenschutzkommission”, SSK) on the rationale behind the currently valid dose limits and dose constraints for workers recommended by the International Commission on Radiological Protection (ICRP). The paper includes a discussion of the reasoning behind current dose limits followed by a discussion of the detriment used by ICRP as a measure for stochastic health effects. Studies on radiation-induced cancer are reviewed because this endpoint represents the most important contribution to detriment. Recent findings on radiation-induced circulatory disease that are currently not included in detriment calculation are also reviewed. It appeared that for detriment calculations the contribution of circulatory diseases plays only a secondary role, although the uncertainties involved in their risk estimates are considerable. These discussions are complemented by a review of the procedures currently in use in Germany, or in discussion elsewhere, to define limits for genotoxic carcinogens. To put these concepts in perspective, actual occupational radiation exposures are exemplified with data from Germany, for the year 2012, and regulations in Germany are compared to the recommendations issued by ICRP. Conclusions include, among others, considerations on radiation protection concepts currently in use and recommendations of the SSK on the limitation of annual effective dose and effective dose cumulated over a whole working life.     

Evidence for significant heritability of apoptotic and cell cycle responses to ionising radiation

Genetic factors are likely to affect individual cancer risk, but few quantitative estimates of heritability are available. Public health radiation protection policies do not in general take this potentially important source of variation in risk into account. Two surrogate cellular assays that relate to cancer susceptibility have been developed to gain an insight into the role of genetics in determining individual variation in radiosensitivity. These flow cytometric assays for apoptosis induction and cell cycle delay following radiation are sufficiently sensitive to distinguish lymphocytes from a healthy donor population from those of a sample of obligate carriers of ATM mutations (P = 0.01 and P = 0.02, respectively). Analysis of 54 unselected twin pairs (38 dizygotic, 16 monozygotic) indicated much greater intrapair correlation in response in monozygotic than in dizygotic pairs. Structural equation modelling indicated that models including unique environmental factors only fitted the data less well than those incorporating two or more of additive genetic factors, common environmental factors and unique environmental factors. A model incorporating additive genetic factors and unique environmental factors yielded estimates of heritability for the two traits of 68% (95% CI 40–82%, cell cycle) and 59% (95% CI 22–79%, apoptosis). Thus, these data suggest that genetic factors contribute significantly to human variation in these two measures of radiosensitivity that relate to cancer susceptibility.     

General and specific mechanisms of biochemical interactions between plants

There exist two main mechanisms of allelopathy: 1) direct transfer of metabolites between neighbouring plants during their life and 2) accumulation and transformation of bioactive substances in the environment with their subsequent influence on higher plants. The latter mechanism is similar to that causing soil sickness or soil toxicity. Allelochemicals affect all functions of the living system: photosynthesis, respiration, mineral nutrition, transpiration, immunity, and growth. The initial biochemical effect of allelochemicals seems to be on the synthesis of protein mediated by RNA/DNA. Knowledge of the mechanisms of concrete signals during realization of hereditary codes would serve as a powerful tool for the improvement of crop plant development and productivity. This paper is based on and employs a broader definition of allelopathy than most other contributions to this collection of colloquium reports, in that it includes all interactions of plants, not merely inhibitory ones.     

肺癌中piR-932的表达及其生物学行为机制研究

目的研究肺癌干细胞中piR-932的表达,以期为肺癌的治疗提供参考。方法应用piRNA芯片检测肺癌于细胞中piRNAs的表达,应用基因芯片检测肺癌干细胞中基因表达的差异,并检测表达下调的基因之一——Latexin的甲基化程度。结果经诱导至EMT的肺癌干细胞中,piR-932的表达明显增高,而Latexin的表达显著下降,并且Latexin启动子区域CpG岛发生了明显的甲基化。结论piR-932可能通过促进Latexin的甲基化而正渊节肺癌干细胞的EMT过程,它可作为肺癌治疗的一个潜在靶点。     

Strong association between pseudogenization mechanisms and gene sequence length

 

Bacteriocins are peptide antibiotics from ribosomally translated precursors, produced by bacteria often through extensive post-translational modification. Minimal sequence conservation, short gene lengths, and low complexity sequence can hinder bacteriocin identification, even during gene calling, so they are often discovered by proximity to accessory genes encoding maturation, immunity, and export functions. This work reports a new subfamily of putative thiazole-containing heterocyclic bacteriocins. It appears universal in all strains of Bacillus anthracis and B. cereus, but has gone unrecognized because it is always encoded far from its maturation protein operon. Patterns of insertions and deletions among twenty-four variants suggest a repeating functional unit of Cys-Xaa-Xaa.

Reviewers

This article was reviewed by Andrei Osterman and Lakshminarayan Iyer.     

Strong association between pseudogenization mechanisms and gene sequence length

   

Pseudogenes arise from the decay of gene copies following either RNA-mediated duplication (processed pseudogenes) or DNA-mediated duplication (nonprocessed pseudogenes). Here, we show that long protein-coding genes tend to produce more nonprocessed pseudogenes than short genes, whereas the opposite is true for processed pseudogenes. Protein-coding genes longer than 3000 bp are 6 times more likely to produce nonprocessed pseudogenes than processed ones.