In chloroplasts, post-translational modification by phosphorylation of apoproteins of chloroplast light-harvesting complex II is initiated when plastoquinone becomes reduced. Phosphorylation of LHC II causes a subpopulation of LHC II molecules to move from photosystem II to photosystem I, redistributing absorbed excitation energy so that the rates of photochemical conversion in the two reaction centres are made equal. Thus a CPI-613 predominance of the reduced form of plastoquinone, plastoquinol, initiates a self-correcting response, a transition to a state of adaptation to light otherwise absorbed primarily by photosystem II. The phospho-LHC II phosphatase required for the state 1 transition has been identified as PPH1 also termed TAP38. As distinct from state transitions, changes in the quantity of photosystem I relative to that of photosytem II are also induced by changes in spectral composition of light absorbed.

Therefore the MTAs discovered by WMC808 and GWM4145 are possibly caused by an allele of Rht5. Gene Rht9 was mapped to chromosome arm 5AL in the Chuan Mai 18 6Mara population and linked to marker BARC151. The significant MTAs at both sites, on chromosomes 7AS and 4AL, may be caused by the respective KAO-genes, since a KAO-gene has been described as Dwarf3 gene in maize. On chromosome 7AS a large significant cluster of SNP markers was detected which had synteny to the rice gene OsKAO on rice chromosome 6, the syntenic locus to KAO-A1 in wheat. The Rht1 mutant phenotypes were found to increase harvest index and grain yield and were therefore introduced in many commercial wheat varieties around the world. But also some negative effects, like decreased seedling vigour and shorter coleoptiles were reported for these GA-insensitive dwarfing genes. Beneficial effects for the Rht1 wild type alleles were reported in drought environments.

All of these changes were reminiscent of the disease features associated with IMR in humans. We also show consistently that the level of circulating troponins increased to 106.8 ng/ml at 30 days post-implantation of an ameroid constrictor, implying that the ameroid constrictor had induced the cellular pathological changes. Furthermore, the eccentric “drop-like” jets indicative of mitral regurgitation near the left atrial wall, abnormal movement of the mitral muscle, and gradual increase in left ventricular systolic and diastolic volumes as well as left atrial volumes, further indicated that the regurgitation jet was caused by an ischemic mitral regurgitation, a critical feature observed in the natural history of IMR in humans. Moreover, brain natriuretic peptide, which is a cardiac neurohormone secreted from ventricles in response to ventricular volume expansion and pressure overload, was also assessed in pigs. Blood BNP levels can be used as a biochemical marker for congestive heart failure.