Photodamage and Photoprotection of Phytoplankton photobiology.info/Hader.html Aquatic ecosystems cover about 70% of the surface of our globe. They produce an amount of biomass that is equal to all the terrestrial ecosystems (e.g., forests and grassland, agricultural areas and tundras and taigas) taken together. The oceans represent the largest share in the aquatic ecosystems, and all freshwater surfaces combined (lakes, rivers) account for only 0.5%. While macroalgae (kelp) are the major biomass producers in coastal areas, phytoplankton are the predominant players in the open sea. Phytoplankton organisms are in a dilemma: they are forced to move into the photic zone due to their energetic requirements for solar radiation and on the other hand they are affected by excessive solar radiation. Especially short wavelength UV bleaches the photosynthetic pigments and breaks down important other biomolecules including proteins and lipids. Under the exposure of solar radiation chromophores form reactive oxygen species (ROS) which affect structural and functional components of the cell. Especially the genetic material of the cell, the DNA, is a major target of solar radiation. Exposure to solar UV-B radiation (280 – 315 nm) results in the formation of dimers of adjacent thymine or cytosine bases in the DNA molecule, Figure 8. If these chemical modifications are not corrected they constitute mutations or result in damage and death of the organisms. Fortunately, cells have developed powerful mechanisms to identify and repair these UV-induced lesions. One of the mechanisms involves an enzyme (photolyase) which uses the energy of a UV-A/blue photon to break the dimer. Following the frequency of dimer formation in a population of planktonic organisms shows a drastic increase during daytime, especially if the organisms are located close to the surface. In the late afternoon and evening hours these lesions are repaired. The leftover lesions are then repaired overnight using different molecular mechanisms (e.g. excision repair). A critical situation arises when there is a carryover of lesions not repaired before the next exposure, so that there is a build up of dimers in the genetic material. Other protective mechanisms of phytoplankton rely on the absorption of solar UV by a cellular “sunscreen”. Many phytoplankton (but also macroalgae) produce one or more mycosporine-like amino acids (MAA) which absorb in the UV range. These substances are located in the outer cytoplasmic layers and prevent up to 7 out of 10 UV photons from reaching the central targets (e.g. the DNA in the nucleus). The MAAs can be extracted from the cells, Figure 9, and separated by HPLC, Figure 10. ### ~~~~~~~~~~~~~~~~ Thymidine Dimers are produced when adjacent thymidine residues are covalently linked by exposure to ltraviolet radiation. Covalent linkage may result in the dimer being replicated as a single base, which results in a frameshift mutation.. https://mun.ca/biology/scarr/Thymine-Thymine_Dimers.html ### ~~~~~~~~~~~~~~~~ A frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides in a DNA sequence that is not divisible by three. Due to the triplet nature of gene expression by codons, the insertion or deletion can change the reading frame (the grouping of the codons), resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein.[1] A frameshift mutation is not the same as a single-nucleotide polymorphism in which a nucleotide is replaced, rather than inserted or deleted. A frameshift mutation will in general cause the reading of the codons after the mutation to code for different amino acids. The frameshift mutation will also alter the first stop codon (UAA, UGA or UAG) encountered in the sequence. The polypeptide being created could be abnormally short or abnormally long, and will most likely not be functional. en.wikipedia.org/wiki/Frameshift_mutation
Posted on: Tue, 18 Nov 2014 07:02:37 +0000
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