Dynamic Regulatory Processes Research Articles

Low-night temperature increased the photoinhibition of photosynthesis in grapevine ( Vitis vinifera L. cv. Riesling) leaves

Photoinhibition of photosynthesis is a process by which excessive light radiation, which is absorbed by the leaves, results in the inactivation and/or impairment of the chlorophyll-containing reaction centers of the chloroplasts, thus inhibiting photosynthesis. The susceptibility of leaves to photoinhibition is known to be enhanced by additional stress factors, which coincide with the light. In this work, we have studied photoinhibition of photosynthesis in control and low-night temperature (LNT) leaves of grapevine ( Vitis vinifera L. cv. Riesling) under controlled conditions (irradiation of detached leaves to about 1900 μmol m −2 s −1). The degree of photoinhibition was determined by means of the ratio of variable to maximum chlorophyll (Chl) fluorescence ( F v/ F m) and electron transport measurements. The potential efficiency of PSII, F v/ F m declined, F 0 increased significantly in high light (HL) irradiated LNT leaves than in control leaves. In isolated thylakoids, the rate of whole chain and PSII activity markedly decreased in HL irradiated more in leaves of LNT than in leaves of control. A smaller inhibition of PSI activity was also observed in both leaves. The artificial exogenous electron donors DPC, NH 2OH and Mn 2+ failed to restore the HL induced loss of PSII activity in control leaves, while DPC and NH 2OH were restored in LNT leaves. It is concluded that HL in LNT leaves inactivates both acceptor and donor side of PSII whereas it does at the acceptor side only in control leaves. Quantification of the PSII reaction center protein D1 and 33 kDa protein water splitting complex following HL exposure of leaves showed pronounced differences between control and LNT. The marked loss of PSII activity in HL irradiated LNT leaves were due to the marked loss of D1 and 33 kDa proteins. The high degree of photoinhibition observed in LNT leaves probably represents a dynamic regulatory process protecting the photosynthetic apparatus from severe damage by excess light.

Brain pathways controlling food intake and body weight.

Evidence has existed for more than 50 years in support of the hypothesis that body energy stored in the form of fat is homeostatically regulated. Implicit in this concept is the existence of a biological system that operates dynamically over time to match cumulative energy intake to energy expenditure. For example, to compensate for weight loss induced by energy restriction, animals must enter a period of positive energy balance (i.e., energy intake greater than energy expenditure) that is sustained for as long as it takes to correct the deficit in body fat stores. Having reached this point, the animal must return to a state of neutral energy balance if stable fat mass is to be maintained. The identification of neuronal circuits in the hypothalamus that, when activated, exert potent, unidirectional effects on energy balance provides a cornerstone of support for this model. The additional finding that these central effector pathways are regulated by humoral signals generated in proportion to body fat stores, including the hormones insulin and leptin, helps to round out the picture of how energy homeostasis is achieved. The goal of this overview is to highlight the evidence that specific subsets of hypothalamic neurons containing specific signaling molecules participate in this dynamic regulatory process, and to put these observations in the larger context of a biological system that controls body adiposity.

High susceptibility to photoinhibition of young leaves of tropical forest trees

Photoinhibition of photosynthesis was studied in young (but almost fully expanded) and mature canopy sun leaves of several tropical forest tree species, both under controlled conditions (exposure of detached leaves to about 1.8 mmol photons·m-2·s-1) and in the field. The degree of photoinhibition was determined by means of the ratio of variable to maximum chlorophyll (Chl) fluorescence emission (FV/FM) and also by gas-exchange measurements. For investigations in situ, young and mature leaves with similar exposure to sunlight were compared. The results show a consistently higher degree of photoinhibition in the young leaves. In low light, fast recovery was observed in both types of leaves in situ, as well as in the laboratory. The fluorescence parameter 1 — FS/F′M (where FS = stationary fluorescence and f′M = maximum fluorescence during illumination) was followed in situ during the course of the day in order to test its suitability as a measure of the photosynthetic yield of photosystem II (PSII). Electron-transport rates were calculated from these fluorescence signals and compared with rates of net CO2 assimilation. Measurements of diurnal changes in PSII ‘yield’ confirmed the increased susceptibility of young leaves to photoinhibition. Calculated electron transport qualitatively reflected net CO2 uptake in situ during the course of the day. Photosynthetic pigments were analyzed in darkened and illuminated leaves. Young and mature leaves showed the same Chl a/b ratio, but young leaves contained about 50% less Chl a + b per unit leaf area. The capacity of photosynthetic O2 evolution per unit leaf area was decreased to a similar extent in young leaves. On a Chl basis, young leaves contained more α-carotene, more xanthophyll cycle pigments and, under strong illumination, more zeaxanthin than mature leaves. The high degree of reversible photoinhibition observed in these young sun leaves probably represents a dynamic regulatory process protecting the photosynthetic apparatus from severe damage by excess light.

1.25-Dihydroxyvitamin D 3 increases secretion of inhibitory insulin-like growth factor binding protein-4 and inhibits mitogenesis in osteoblastic cells

Extracellular potassium concentration, [K+]o, is a major determinant of neuronal excitability. In the healthy brain, [K+]o levels are tightly controlled. During seizures, [K+]o increases up to 15 mM and is thought to cause seizures due to its depolarizing effect. Although astrocytes have been suggested to play a key role in the redistribution (or spatial buffering) of excess K+ through Connexin-43 (Cx43)-based Gap Junctions (GJs), the relation between this dynamic regulatory process and seizure generation remains unknown. Here we contrasted the role of astrocytic GJs and hemichannels by studying the effect of GJ and hemichannel blockers on [K+]o regulation in vivo. [K+]o was measured by K+-sensitive microelectrodes. Neuronal excitability was estimated by local field potential (LFP) responses to forepaw stimulation and changes in the power of resting state activity. Starting at the baseline [K+]o level of 1.61 ± 0.3 mM, cortical microinjection of CBX, a broad spectrum connexin channel blocker, increased [K+]o to 11 ± 3 mM, Cx43 GJ/hemichannel blocker Gap27 increased it from 1.9 ± 0.7 to 9 ± 1 mM. At these [K+]o levels, no seizures were observed. Cx43 hemichannel blockade with TAT-Gap19 increased [K+]o by only ~ 1 mM. Microinjection of 4-aminopyridine, a known convulsant, increased [K+]o to ~ 10 mM and induced spontaneously recurring seizures, whereas direct application of K+ did not trigger seizure activity. These findings are the first in vivo demonstration that astrocytic GJs are major determinants for the spatial buffering of [K+]o and that an increase in [K+]o alone does not trigger seizures in the neocortex.