Organisms respond to stress through activation of a wide variety of biochemical and molecular mechanisms. Stresses that damage DNA either directly or indirectly trigger activation of the cell-cycle control systems, DNA repair and apoptosis mechanisms. These mechanisms are directed towards eliminating DNA damage and preventing the burden of mutations in organisms and their progeny. Several independent observations suggest that response to DNA-damaging and non-DNA-damaging stresses includes changes in directly exposed cells and/or tissues as well as changes in neighbouring non-exposed naïve ones. Moreover, several studies show that non-exposed organisms and exposed organisms housed together exhibit similar changes in their metabolism and genome stability. The response of non-exposed biological units (cells/tissues/organisms) is known as the bystander effect. There have been proposed various models attempting to explain the phenomenon of bystander response and its mechanisms, including a reactive oxygen species model, hormone models, small RNA-based models and models of other small signalling molecules.
Stress, undoubtedly, is a powerful force that plays a crucial role in evolution shaping the genomes of various organisms. For a long time, a mutation-based genetic mechanism was believed to be the only possible way that could lead to species diversity and was responsible for potential adaptation to stress. Several recent reports suggest, however, that organisms are able to respond to the environment through heritable but reversible changes in their DNA, the chromatin and a small non-coding RNA pool. These changes are known as epigenetic changes. It is hypothesized that organisms can acquire the memory of stress exposure by passing stress-specific epigenetic marks onto their progeny. Changes in the progeny of stressed organisms are known as transgenerational effects. Transgenerational effects have been well documented in the progeny of exposed fathers. Nevertheless, the potential maternal heritability of transgenerational effects still remains to be established. Indeed, in exposed females, only changes in the F3 generation are considered to be truly heritable.
In this Research Topic issue, we describe the intriguing phenomena of bystander and transgenerational responses to various stresses. We will report on observations of bystander effects in cells, tissues and whole organisms and describe the possible genetic and epigenetic regulatory mechanisms involved in the response of bystander units. While talking about the phenomenon of transgenerational response, we will provide examples of heritable and non-heritable transgenerational effects in various organisms. A specific emphasis will be given to transgenerational changes in response to physical and chemical agents, various disease therapies and behavioural changes.
Organisms respond to stress through activation of a wide variety of biochemical and molecular mechanisms. Stresses that damage DNA either directly or indirectly trigger activation of the cell-cycle control systems, DNA repair and apoptosis mechanisms. These mechanisms are directed towards eliminating DNA damage and preventing the burden of mutations in organisms and their progeny. Several independent observations suggest that response to DNA-damaging and non-DNA-damaging stresses includes changes in directly exposed cells and/or tissues as well as changes in neighbouring non-exposed naïve ones. Moreover, several studies show that non-exposed organisms and exposed organisms housed together exhibit similar changes in their metabolism and genome stability. The response of non-exposed biological units (cells/tissues/organisms) is known as the bystander effect. There have been proposed various models attempting to explain the phenomenon of bystander response and its mechanisms, including a reactive oxygen species model, hormone models, small RNA-based models and models of other small signalling molecules.
Stress, undoubtedly, is a powerful force that plays a crucial role in evolution shaping the genomes of various organisms. For a long time, a mutation-based genetic mechanism was believed to be the only possible way that could lead to species diversity and was responsible for potential adaptation to stress. Several recent reports suggest, however, that organisms are able to respond to the environment through heritable but reversible changes in their DNA, the chromatin and a small non-coding RNA pool. These changes are known as epigenetic changes. It is hypothesized that organisms can acquire the memory of stress exposure by passing stress-specific epigenetic marks onto their progeny. Changes in the progeny of stressed organisms are known as transgenerational effects. Transgenerational effects have been well documented in the progeny of exposed fathers. Nevertheless, the potential maternal heritability of transgenerational effects still remains to be established. Indeed, in exposed females, only changes in the F3 generation are considered to be truly heritable.
In this Research Topic issue, we describe the intriguing phenomena of bystander and transgenerational responses to various stresses. We will report on observations of bystander effects in cells, tissues and whole organisms and describe the possible genetic and epigenetic regulatory mechanisms involved in the response of bystander units. While talking about the phenomenon of transgenerational response, we will provide examples of heritable and non-heritable transgenerational effects in various organisms. A specific emphasis will be given to transgenerational changes in response to physical and chemical agents, various disease therapies and behavioural changes.
