Increased growing-season productivity drives earlier autumn leaf senescence in temperate trees

Science ◽  
2020 ◽  
Vol 370 (6520) ◽  
pp. 1066-1071 ◽  
Author(s):  
Deborah Zani ◽  
Thomas W. Crowther ◽  
Lidong Mo ◽  
Susanne S. Renner ◽  
Constantin M. Zohner
Keyword(s):  
Leaf Senescence ◽  
Critical Role ◽  
Biotic Interactions ◽  
Growing Season ◽  
Environmental Drivers ◽  
Light Levels ◽  
Temperate Trees ◽  
Autumn Leaf

Changes in the growing-season lengths of temperate trees greatly affect biotic interactions and global carbon balance. Yet future growing-season trajectories remain highly uncertain because the environmental drivers of autumn leaf senescence are poorly understood. Using experiments and long-term observations, we show that increases in spring and summer productivity due to elevated carbon dioxide, temperature, or light levels drive earlier senescence. Accounting for this effect improved the accuracy of senescence predictions by 27 to 42% and reversed future predictions from a previously expected 2- to 3-week delay over the rest of the century to an advance of 3 to 6 days. These findings demonstrate the critical role of sink limitation in governing the end of seasonal activity and reveal important constraints on future growing-season lengths and carbon uptake of trees.

The effect of growing-season productivity on autumn phenology in temperate trees

2021 ◽  
Author(s):  
Constantin Zohner
Keyword(s):  
Leaf Senescence ◽  
Photosynthetic Activity ◽  
Biotic Interactions ◽  
Growing Season ◽  
Carbon Uptake ◽  
Extrinsic Factors ◽  
Growing Season Length ◽  
Temperate Trees ◽  
Autumn Leaf ◽  
Physiological Constraint

<p><strong>Phenological shifts in plants greatly affect biotic interactions and lead to multiple feedbacks to the climate system</strong><strong>. Increases in growing-season length under warmer climates are expected to drive changes in water, nutrient, and energy fluxes as well as enhancing ecosystem carbon uptake</strong><strong>. Yet, future trajectories of growing-season lengths remain highly uncertain because the intrinsic and extrinsic factors triggering autumn leaf senescence, including lagged effects of spring and summer productivity</strong><strong>, are poorly understood. Here, we use 434,226 spring leaf-out and autumn leaf senescence observations of temperate trees from Central Europe between 1948 and 2015 to test the effect of seasonal photosynthetic activity on leaf senescence, thereby exploring the extent to which growing-season lengths are internally regulated by constraints on productivity. We found that spring and summer productivity was a critical driver of autumn phenology, with earlier leaf senescence in years with high seasonal photosynthetic activity. Our new process-based model, incorporating information on growing-season photosynthesis, increased the accuracy of existing autumn phenology models by 22–61%. Furthermore, the physiological constraint of growing-season photosynthesis reversed the predictions of autumn phenology over the rest of the century. </strong><strong>While current phenology models predict that leaf senescence will occur 7–19 days later </strong><strong>by the end of the 21<sup>st</sup> century</strong><strong>, </strong><strong>we estimate that leaf senescence will, in fact, advance by 3–6 days</strong><strong>.</strong><strong> </strong><strong>Our results reveal important constraints on future growing-season lengths and the carbon uptake potential of temperate trees and enhance our capacity to forecast long-term changes in ecosystem functioning, which is critical to improve our understanding of Earth System dynamics in response to climate change.</strong></p>

scholarly journals Response to Comment on “Increased growing-season productivity drives earlier autumn leaf senescence in temperate trees”

Science ◽  
2021 ◽  
Vol 371 (6533) ◽  
pp. eabg2679
Author(s):  
Deborah Zani ◽  
Thomas W. Crowther ◽  
Lidong Mo ◽  
Susanne S. Renner ◽  
Constantin M. Zohner
Keyword(s):  
Leaf Senescence ◽  
Growing Season ◽  
Temperate Trees ◽  
Free Air ◽  
Autumn Leaf ◽  
Autumn Senescence

Our study showed that increases in seasonal productivity drive earlier autumn senescence of temperate trees. Norby argues that this finding is contradicted by observations from free-air CO2 enrichment (FACE) experiments, where elevated CO2 has been found to delay senescence in some cases. We provide a detailed answer showing that the results from FACE studies are in agreement with our conclusions.

scholarly journals Comment on “Increased growing-season productivity drives earlier autumn leaf senescence in temperate trees”

Science ◽  
2021 ◽  
Vol 371 (6533) ◽  
pp. eabg1438 ◽  
Author(s):  
Richard J. Norby
Keyword(s):  
Leaf Senescence ◽  
Growing Season ◽  
Research Articles ◽  
Deciduous Tree ◽  
Temperate Trees ◽  
Free Air ◽  
Autumn Leaf

Zani et al. (Research Articles, 27 November 2020, p. 1066) propose that enhancement of deciduous tree photosynthesis in a CO2-enriched atmosphere will advance autumn leaf senescence. This premise is not supported by consistent observations from free-air CO2 enrichment (FACE) experiments. In most FACE experiments, leaf senescence or abscission was not altered or was delayed in trees exposed to elevated CO2.

scholarly journals Programmed chloroplast destruction during leaf senescence involves 13-lipoxygenase (13-LOX)

2016 ◽  
Vol 113 (12) ◽  
pp. 3383-3388 ◽  
Author(s):  
Armin Springer ◽  
ChulHee Kang ◽  
Sachin Rustgi ◽  
Diter von Wettstein ◽  
Christiane Reinbothe ◽  
...  
Keyword(s):  
Leaf Senescence ◽  
Critical Role ◽  
Transit Peptide ◽  
Physiological Changes ◽  
Pathogen Defense ◽  
Chloroplast Transit Peptide ◽  
Selective Destruction ◽  
Plastid Envelope ◽  
Volatile Aldehydes

Leaf senescence is the terminal stage in the development of perennial plants. Massive physiological changes occur that lead to the shut down of photosynthesis and a cessation of growth. Leaf senescence involves the selective destruction of the chloroplast as the site of photosynthesis. Here, we show that 13-lipoxygenase (13-LOX) accomplishes a key role in the destruction of chloroplasts in senescing plants and propose a critical role of its NH2-terminal chloroplast transit peptide. The 13-LOX enzyme identified here accumulated in the plastid envelope and catalyzed the dioxygenation of unsaturated membrane fatty acids, leading to a selective destruction of the chloroplast and the release of stromal constituents. Because 13-LOX pathway products comprise compounds involved in insect deterrence and pathogen defense (volatile aldehydes and oxylipins), a mechanism of unmolested nitrogen and carbon relocation is suggested that occurs from leaves to seeds and roots during fall.

Persistent Pulmonary Hypertension of the Newborn: Role of Nitric Oxide

1995 ◽  
Vol 10 (6) ◽  
pp. 270-282
Author(s):  
Stella Kourembanas
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Structural Changes ◽  
Critical Role ◽  
Persistent Pulmonary Hypertension ◽  
Cell Contractility ◽  
Vasoactive Mediators ◽  
Nitric Oxide Therapy

Persistent pulmonary hypertension of the newborn (PPHN) is a common cause of respiratory failure in the full-term neonate. Molecular and cellular studies in vascular biology have revealed that endothelial-derived mediators play a critical role in the pathogenesis and treatment of PPHN. Endothelial-derived vasoconstrictors, like endothelin, may increase smooth muscle cell contractility and growth, leading to the physiologic and structural changes observed in the pulmonary arterioles of infants with this disease. On the other hand, decreased production of the endothelial-derived relaxing factor, nitric oxide, may exacerbate pulmonary vasoreactivity and lead to more severe pulmonary hypertension. Exogenous (inhaled) nitric oxide therapy reduces pulmonary vascular resistance and improves oxygenation. The safety and efficacy of this therapy in reducing the need for extracorporeal membrane oxygenation and decreasing long-term morbidity is being tested in several trials nationally and abroad. Understanding the basic mechanisms that regulate the gene expression and production of these vasoactive mediators will lead to improved preventive and therapeutic strategies for PPHN.

scholarly journals THE CRITICAL ROLE OF THE HEALTHCARE SYSTEM ON LONG-TERM CARE ADMISSIONS OF PEOPLE WITH DEMENTIA

2017 ◽  
Vol 1 (suppl_1) ◽  
pp. 969-969
Author(s):  
N. Donnelly ◽  
N. Humphries ◽  
A. Hickey ◽  
F. Doyle
Keyword(s):  
Healthcare System ◽  
Long Term Care ◽  
Critical Role ◽  
Term Care ◽  
People With Dementia

TGF-β1-Induced Long-Term Changes in Neuronal Excitability in Aplysia Sensory Neurons Depend on MAPK

2006 ◽  
Vol 95 (5) ◽  
pp. 3286-3290 ◽  
Author(s):  
Jeannie Chin ◽  
Rong-Yu Liu ◽  
Leonard J. Cleary ◽  
Arnold Eskin ◽  
John H. Byrne
Keyword(s):  
Sensory Neuron ◽  
Transforming Growth Factor Beta ◽  
Neuronal Excitability ◽  
Transforming Growth Factor ◽  
Critical Role ◽  
Camp Response Element Binding ◽  
Long Term Changes ◽  
Tgf Β1

Transforming growth factor beta-1 (TGF-β1) plays important roles in the early development of the nervous system and has been implicated in neuronal plasticity in adult organisms. It induces long-term increases in sensory neuron excitability in Aplysia as well as a long-term enhancement of synaptic efficacy at sensorimotor synapses. In addition, TGF-β1 acutely regulates synapsin phosphorylation and reduces synaptic depression induced by low-frequency stimuli. Because of the critical role of MAPK in other forms of long-term plasticity in Aplysia, we examined the role of MAPK in TGF-β1-induced long-term changes in neuronal excitability. Prolonged (6 h) exposure to TGF-β1 induced long-term increases in excitability. We confirmed this finding and now report that exposure to TGF-β1 was sufficient to activate MAPK and increase nuclear levels of active MAPK. Moreover, TGF-β1 enhanced phosphorylation of the Aplysia transcriptional activator cAMP response element binding protein (CREB)1, a homologue to vertebrate CREB. Both the TGF-β1-induced long-term changes in neuronal excitability and the phosphorylation of CREB1 were blocked in the presence of an inhibitor of the MAPK cascade, confirming a role for MAPK in long-term modulation of sensory neuron function.

Activity-dependent induction of functional secretory properties at cultured neuromuscular synapses of Helisoma

1996 ◽  
Vol 76 (4) ◽  
pp. 2635-2643 ◽  
Author(s):  
J. C. Poyer ◽  
M. J. Zoran
Keyword(s):  
Cell Culture ◽  
Critical Role ◽  
Muscle Fibers ◽  
Pond Snail ◽  
Culture Dish ◽  
Neuromuscular Synapses ◽  
Neuronal Processes ◽  
Activity Dependent

1. The role of activity-dependent mechanisms in target-mediated induction of secretory properties was investigated at regenerating neuromuscular synapses of the American pond snail, Helisoma trivolvis, in cell culture. 2. Identified motoneurons were isolated into cell culture conditions that promoted neurite outgrowth. Buccal neurons 19 (B19) were cultured alone for 2 days, at which time dissociated muscle fibers were manipulated into contact with newly formed neurites. 3. Immediately before the plating of muscle fibers, the sodium channel blocker, tetrodotoxin (TTX), or the acetylcholine receptor antagonist, d-tubocurarine chloride (curare), was added to the culture dish. After 48 h of exposure, the inhibitors were removed by repeated dilution of the culture medium and electrophysiological analyses were performed. 4. Cholinoceptive assay cells were manipulated into contact with the presynaptic neurons to assess secretory properties along neuronal processes. Assay cells were used to control for variations in postsynaptic sensitivity that could result from long-term exposure to activity inhibitors. 5. These analyses demonstrated that inhibition of TTX-sensitive presynaptic activity and inhibition of curare-sensitive postsynaptic activation both blocked the induction of excitation-secretion coupling typically induced in these motoneurons by appropriate target contact. Neuron B5, which rapidly acquires functional synaptic properties in vitro, was unaffected in its secretory function by 48 h of activity inhibition. 6. Acquisition of secretory competence was not suppressed due to a reduction in the viability or long-term changes in excitability of the activity-inhibited neurons, as indicated by analyses of electrophysiological properties. 7. Although target-contact and activity both participated in the induction of secretory modifications in neuron B19, target-mediated changes did not involve retrograde effects on presynaptic neuronal excitability. 8. We hypothesize that contact-mediated mechanisms govern the initiation of presynaptic modifications in B19, however, our data indicate that the acquisition of functional excitation-secretion coupling also involves activity-dependent mechanisms. Although the mechanistic role of activity remains undefined, our results suggest that the activation of the target muscle plays a critical role in a retrograde signaling pathway underlying maturation of a functional secretory apparatus in target-contacted neuronal processes.

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