368 research outputs found
Elevated UV-B radiation reduces genome stability in plants
Long-term depletion of the stratospheric ozone layer contributes to an increase in terrestrial solar ultraviolet-B radiation. This has deleterious effects on living organisms, such as DNA damage. When exposed to elevated ultraviolet-B radiation (UV-B; 280–315 nm), plants display a wide variety of physiological and morphological responses characterized as acclimation and adaptation. Here we show, using special sun simulators, that elevated solar UV-B doses increase the frequency of somatic homologous DNA rearrangements in Arabidopsis and tobacco plants. Increases in recombination are accompanied by a strong induction of photolyase and Rad51 gene expression. These genes are putatively involved in major DNA repair pathways, photoreactivation and recombination repair. In mutant Arabidopsis plants that are deficient in photoreactivating ultraviolet-induced cyclobutane pyrimidine dimers, recombination under elevated UV-B regimes greatly exceeds wild-type levels. Our results show that homologous recombination repair pathways might be involved in eliminating UV-B-induced DNA lesions in plants. Thus, increases in terrestrial solar UV-B radiation as forecasted for the early 21st century may affect genome stability in plants
Increased Anion Channel Activity Is an Unavoidable Event in Ozone-Induced Programmed Cell Death
Ozone is a major secondary air pollutant often reaching high concentrations
in urban areas under strong daylight, high temperature and stagnant
high-pressure systems. Ozone in the troposphere is a pollutant that is
harmful to the plant. generation by salicylic and abscisic acids.
Anion channel activation was also shown to promote the accumulation of
transcripts encoding vacuolar processing enzymes, a family of proteases
previously reported to contribute to the disruption of vacuole integrity
observed during programmed cell death.-induced
programmed cell death. Because ion channels and more specifically anion
channels assume a crucial position in cells, an understanding about the
underlying role(s) for ion channels in the signalling pathway leading to
programmed cell death is a subject that warrants future investigation
Scaling Behavior of Human Locomotor Activity Amplitude: Association with Bipolar Disorder
Scale invariance is a feature of complex biological systems, and abnormality of multi-scale behaviour may serve as an indicator of pathology. The hypothalamic suprachiasmatic nucleus (SCN) is a major node in central neural networks responsible for regulating multi-scale behaviour in measures of human locomotor activity. SCN also is implicated in the pathophysiology of bipolar disorder (BD) or manic-depressive illness, a severe, episodic disorder of mood, cognition and behaviour. Here, we investigated scaling behaviour in actigraphically recorded human motility data for potential indicators of BD, particularly its manic phase. A proposed index of scaling behaviour (Vulnerability Index [VI]) derived from such data distinguished between: [i] healthy subjects at high versus low risk of mood disorders; [ii] currently clinically stable BD patients versus matched controls; and [iii] among clinical states in BD patients
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