For this purpose, we sequenced two high light (HL) resistant C. reinhardtii mutants that originated from a forward genetic approach by either spontaneous mutation or ultraviolet (UV) light induced mutagenesis, respectively.
Our results present an apparent paradox regarding the evolutionary history of the Prochlorococcus lineage: the eMIT9313 ecotype, which is restricted from the HOOH-enriched mixed layer by its sensitivity to high light, is more resistant to HOOH than the ecotypes found in high abundance in the mixed layer.
However, it is not shown whether or not RB-treated cells are also resistant to high light or Norflurazon, two conditions known to produce 1O2 in the chloroplasts.
We show that antenna proteins play a dual role in Arabidopsis thaliana Photosystem I photoprotection: first, a Photosystem I with an intact antenna system is more resistant to high light because of a reduced production of reactive oxygen species and, second, antenna chlorophyll-proteins are the first target of high light damages.
The observation that all six TAM mutants are resistant to high light suggests that rather than defects in pigment biosynthesis, where lesions induce photosensitivity [ 40, 41], mutations in the TAM lines likely affect chloroplast biogenesis steps such as those mediated by NAB1, ARSA1, or cpSRP [ 35, 37, 42].
Isolated LHCI showed an even lower resistance to high light, implying that its photoprotective effect requires the interaction with PSI core: PSI-LHCI supercomplex, in fact, is more resistant to light treatment than both individual moieties.
It is worth noting that no decrease in O2 production was observed at very high light conditions (>3,000 μmol photons m-2 s-1), suggesting that these strains are rather resistant to photo-oxidative stress.
LDHS were used as the ultraviolate light resistant materials.
