Alterations in photosynthetic capacity of primary leaves of wheat seedlings in response to ultraviolet-B (UV-B; 280-320 nm; 60 µmol m-2 s-1) exposure alone and in combination with photosynthetically active radiation (PAR; 400-800 nm; 200 µmol m-2 s-1) during different phases of leaf growth and development were assessed. UV-B exposure resulted in a phase-dependent differential loss in photosynthetic pigments, photochemical potential, photosystem 2 (PS2) quantum yield, and in vivo O2 evolution. UV-B exposure induced maximum damage to the photosynthetic apparatus during senescence phase of development. The damages were partially alleviated when UV-B exposure was accompanied by PAR. UV-B induced an enhancement in accumulation of flavonoids during all phases of development while it caused a decline in anthocyanin content during senescence. The differential changes in these parameters demonstrated the adaptation ability of leaves to UV-B stress during all phases of development and the ability was modified in UV-B+ PAR exposed samples. and M. K. Pradhan ... [et al.].
Leaf senescence is always associated with decline in photosynthesis, consequently a loss of cellular sugar. On the other hand, execution of senescence program needs energy and leaves, therefore, tend to collect sugars from other sources to sustain energy homeostasis. This sugar reprogramming induced by loss of sugar involves operation of a complex catabolic network. The exact molecular mechanism of induction and regulation of the network, however, is not fully resolved but the current literature available suggests sugar starvation as a signal for induction of several senescence-associated genes including the genes coding for the enzymes for degradation of cellular constituents and their conversion to respiratory sugars. The late expression of genes coding for the cell wall hydrolases and enhancement in the activity of these enzymes late during senescence are indicative of the cell wall polysaccharides as the last source of sugars to sustain energy homeostasis for execution of the senescence program., B. Biswal, J. K. Pandey., and Obsahuje bibliografické odkazy
Flooding stress (FS) induced changes in pigment and protein contents and in photochemical efficiency of thylakoid membranes of chloroplasts were investigated during senescence of primary leaves of rice seedlings. Leaf senescence was accompanied by loss in 2,6-dichlorophenolindophenol (DCPIP) photoreduction, rate of oxygen evolution, quantum yield of photosystem 2 with an increase in MDA accumulation, and non-photochemical quenching (NPQ) of chlorophyll fluorescence. These changes were further aggravated when the leaves during this period experienced FS. The increase in NPQ value under stress may indicate photosynthetic adaptation to FS. and S. K. Mishra ... [et al.].
In clusterbean leaves UV-B radiation caused a reduction in contents of chlorophylls and carotenoids and in the efficiency of photosystem 2 photochemistry. The degree of damage was reduced when UV-A accompanied the UV-B radiation. This indicates the counteracting effect of UV-A radiation against UV-B-induced impairment. and S. Gartia ... [et al.].
Seedlings of Cyamopsis tetragonoloba were grown on Petri dishes either in water or water plus 3 % PEG-6000 to induce water stress. The senescing cotyledons experiencing the stress exhibited loss in contents of leaf proteins and chlorophyll (Chl) and a decline in oxygen evolution. The effect of PEG treatment was more pronounced at moderate (MI) than low (LI) irradiance. The stress-induced loss in the activity of superoxide dismutase and increase in the thylakoid lipid peroxidation accompanied a change in the physical status of the bilayer membrane as demonstrated by an enhancement of room temperature Chl a fluorescence polarization and decrease in energy transfer efficiency in pigment assembly. This resulted in a sustained decrease in photosystem 2 activity blocking channels of energy utilization. The absorbed quanta, thus unutilized, were excess even at MI, leading to photoinhibitory response. and P. M. Deo, U. C. Biswal, B. Biswal.