Low temperature effects on grapevine photosynthesis: the role of inorganic phosphate

2004 ◽  
Vol 31 (8) ◽  
pp. 789 ◽  
Author(s):  
Luke Hendrickson ◽  
Wah Soon Chow ◽  
Robert T. Furbank

The photosynthetic response of grapevine leaves (Vitis vinifera L. cv. Riesling) to low temperature was studied to determine the role of end-product limitation and orthophosphate (Pi) recycling to the chloroplast under these conditions. As reported previously, the response of photosynthesis in air to stomatal conductance declined at temperatures below 15°C, suggesting that at low temperatures inhibition of photosynthesis in grapevine has a strong non-stomatal component. Stimulation of carbon assimilation at ambient CO2 by reducing O2 from 21 to 2 kPa, O2 declined to zero below 15°C, a phenomenon often associated with a restriction in photosynthesis due to end-product-synthesis limitation. This stimulation could be restored by feeding Pi. Photosynthesis in leaf disks at both high and low irradiances in non-photorespiratory conditions (1% CO2) was highly sensitive to reductions in temperature. Below 15°C, feeding Pi caused a large stimulation of photosynthetic O2 evolution. Metabolite measurements indicated that despite a decline in Rubisco carbamylation state, ribulose 1,5-bisphosphate (RuBP) levels dropped at low temperature and the ratio of 3-phosphoglycerate (3-PGA) to triose phosphate (TP) remained largely unchanged. These results suggest that grapevine-leaf photosynthesis is severely restricted at low temperature by non-stomatal mechanisms. The return of Pi to the chloroplast plays an important role in this limitation but a coordinated set of regulatory processes maintain a homeostasis of phosphorylated sugar levels.

1978 ◽  
Vol 5 (3) ◽  
pp. 239 ◽  
Author(s):  
GP Arron ◽  
DA Day ◽  
SD Grover ◽  
GG Laties

The plant hormone ethylene had no apparent effect on the redox state of the respiratory chain components of sweet potato mitochondria during oxidation of succinate. Low temperature e.p.r. spectra of sweet potato mitochondria, in various respiratory states, were not altered by the presence of ethylene. Oxygen uptake rates and ADP/O ratios of sweet potato mitochondria oxidising malate or succinate were also not affected by ethylene. The role of ethylene in the stimulation of respiration in plant tissues is discussed.


1977 ◽  
Vol 72 (2) ◽  
pp. 456-469 ◽  
Author(s):  
R R Whitesell ◽  
R A Johnson ◽  
H L Tarpley ◽  
D M Regen

The plant lectin, concanavalin A (Con-A), and the ionophore, A-23187 (specific for divalent cations), stimulated glucose transport in rat thymocytes. Con-A stimulation developed more slowly and was somewhat less extensive than that of stimulation developed more slowly and was somewhat less extensive than that of A-23187. Both responses showed saturation dose dependencies. The two responses were poorly additive, suggesting that A-23187 may saturate regulatory processes shared by the two stimulatory mechanisms. Doses of methylisobutylxanthine (MIX) and prostaglandin E2 which raised adenosine 3':5'-monophosphate (cAMP) levels in these cells also antagonized the Con-A stimulation of glucose transport but did not inhibit basal glucose transport or the A-23187 stimulation. Dibutyryl-cAMP and 8-bromo-cAMP also natagonized Con-A stimulation without inhibiting basal glucose transport. MIX antagonized high Con-A doses about as strongly as it did low Con-A doses, suggesting that MIX did not compete in the Con-A binding step or other process saturable by Con-A. [3H-A1Con-A binding was not affected by MIX. The stimulatory effects of Con-A and A-23187 were reduced by reduction of Ca++ in the medium. Both Con-A and A-23187 enhanced 45Ca++ influx and cellular Ca++ content. The A-23187 dose, which was saturating for glucose transport stimulation, enhanced Ca++ influx and cellular Ca++ content more than did the Con-A dose which was saturating for glucose transport stimulation. The dose fo MIX which specifically antagonized Con-A stimulation of glucose transport proved also to reduce Ca++ influx and cellular Ca++ in the presence of Con-A but not in the presence of A-23187. Thus, glucose transport correlates rather well with cellular Ca++. These results are compatible with the view that Ca++ in a cellular compartment can promote glucose transport, the Con-A's enhancement of Ca++ entry contributes to its stimulation of glucose transport, and the MIX antagonized Con-A action at least partly by reducing Ca++ entry. The action of MIX is apparently mediated by cAMP.


Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.


Author(s):  
Maria M. Wong

Individuals with alcohol problems have well-described disturbances of sleep, but the development of these disturbances both before and after the onset of problem drinking is poorly understood. This chapter first discusses sleep physiology and its measurement in humans. It then examines the functions of sleep and its role in development. Next, it reviews recent research on the relationship between sleep and alcohol use and related problems. Whereas sleep problems (e.g., difficulties falling or staying asleep) increase the risk of early onset of alcohol use and related problems, sleep rhythmicity promotes resilience to the development of alcohol use disorder and problem substance use. Based on existing research, this chapter proposes a theoretical model of sleep and alcohol use, highlighting the role of self-regulatory processes as mediators of this relationship.


Author(s):  
Argyris Arnellos

The emphasis on the collaborative dimension of life overlooks the importance of biological individuals (conceived of as integrated, self-maintaining organizations) in the build-up of more complex collaborative networks in the course of evolution. This chapter proposes a process-based organizational ontology for biology, according to which the essential features of unicellular organismicality are captured by a self-maintaining organization of processes integrated by means of a special type of collaboration (realized through regulatory processes entailing an indispensable interdependence) between its constitutive and its interactive aspects. This ontology is then used to describe different types of collaborations among cells and to suggest the type that yields a multicellular organism. The proposed organizational framework enables us to critically assess hypercollaborative views of life, especially issues related to the distinction between biological individuals and organisms and between life and non-life, without however underestimating the central biological role of collaboration.


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