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Connecting proline metabolism and signaling pathways in plant senescence.

Zhang L, Becker DF - Front Plant Sci (2015)

Bottom Line: Proline metabolism is manipulated under stress by multiple and complex regulatory pathways and can profoundly influence cell death and survival in microorganisms, plants, and animals.Though the effects of proline are mediated by diverse signaling pathways, a common theme appears to be the generation of reactive oxygen species (ROS) due to proline oxidation being coupled to the respiratory electron transport chain.Future studies focusing on the mechanisms by which proline metabolic shifts occur during senescence may lead to novel methods to rescue crops under stress and to preserve post-harvest agricultural products.

View Article: PubMed Central - PubMed

Affiliation: Redox Biology Center, Department of Biochemistry, University of Nebraska-Lincoln , Lincoln, NE, USA.

ABSTRACT
The amino acid proline has a unique biological role in stress adaptation. Proline metabolism is manipulated under stress by multiple and complex regulatory pathways and can profoundly influence cell death and survival in microorganisms, plants, and animals. Though the effects of proline are mediated by diverse signaling pathways, a common theme appears to be the generation of reactive oxygen species (ROS) due to proline oxidation being coupled to the respiratory electron transport chain. Considerable research has been devoted to understand how plants exploit proline metabolism in response to abiotic and biotic stress. Here, we review potential mechanisms by which proline metabolism influences plant senescence, namely in the petal and leaf. Recent studies of petal senescence suggest proline content is manipulated to meet energy demands of senescing cells. In the flower and leaf, proline metabolism may influence ROS signaling pathways that delay senescence progression. Future studies focusing on the mechanisms by which proline metabolic shifts occur during senescence may lead to novel methods to rescue crops under stress and to preserve post-harvest agricultural products.

No MeSH data available.


Related in: MedlinePlus

Potential linkages between proline metabolism and signaling pathways in petal and leaf senescence. Petal senescence (A): Aging induced petal senescence results in ROS accumulation and sugar depletion. SnRK1, activated in response to depleted sugar, is proposed to induce PRODH1/2 expression via bZIP1, bZIP11, and bZIP53. Upregulation of PRODH1/2 expression would be predicted to generate ATP thereby attenuating increases in ADP/ATP. PRODH activity is also expected to generate ROS as a by-product, possibly leading to activation of MPK20 and increased Mn-SOD activity. Enhanced Mn-SOD activity would help diminish accumulated ROS and oxidative damage during petal senescence. Activation of MAPK pathways by ROS would induce expression of antioxidant enzymes and petal abscission. Leaf senescence (B): Leaf senescence can be induced by plant hormones, age and detachment. During age-related senescence, the expression of PRODH2 and P5CDH are induced, suggesting a higher flux of proline catabolism and more glutamate available for nitrogen recycling. In response to H2O2 during hormone-induced senescence, PI3K may down-regulate PRODH1 resulting in less ROS signaling and adaptation to oxidative stress. Also during hormone-induced senescence, phospholipase D (PLD) and its product phosphatidic acid (PA) inhibit P5CS1 expression.
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Figure 2: Potential linkages between proline metabolism and signaling pathways in petal and leaf senescence. Petal senescence (A): Aging induced petal senescence results in ROS accumulation and sugar depletion. SnRK1, activated in response to depleted sugar, is proposed to induce PRODH1/2 expression via bZIP1, bZIP11, and bZIP53. Upregulation of PRODH1/2 expression would be predicted to generate ATP thereby attenuating increases in ADP/ATP. PRODH activity is also expected to generate ROS as a by-product, possibly leading to activation of MPK20 and increased Mn-SOD activity. Enhanced Mn-SOD activity would help diminish accumulated ROS and oxidative damage during petal senescence. Activation of MAPK pathways by ROS would induce expression of antioxidant enzymes and petal abscission. Leaf senescence (B): Leaf senescence can be induced by plant hormones, age and detachment. During age-related senescence, the expression of PRODH2 and P5CDH are induced, suggesting a higher flux of proline catabolism and more glutamate available for nitrogen recycling. In response to H2O2 during hormone-induced senescence, PI3K may down-regulate PRODH1 resulting in less ROS signaling and adaptation to oxidative stress. Also during hormone-induced senescence, phospholipase D (PLD) and its product phosphatidic acid (PA) inhibit P5CS1 expression.

Mentions: The molecular pathways by which proline metabolism is regulated during plant senescence are summarized in Figure 2. The ability of proline to delay senescence in petal and leaf tissues is likely due to protection against oxidative stress that occurs in the aging tissue. In leaf, proline may help redistribute nitrogen to younger tissue whereas in flowers, proline helps counter energy shortages. Further insights into how proline metabolism impacts petal and leaf senescence will require additional studies that connect proline with plant senescence signaling pathways. Exploration of the linkages between proline metabolism and important pathways of plant senescence such as MAPK signaling, the SnRK1-bZIP pathway and PI3K signaling will be valuable targets for future study. Better understanding of proline metabolism in senescing leaves may uncover novel strategies for preserving post-harvest flowers and delaying stress-induced leaf senescence.


Connecting proline metabolism and signaling pathways in plant senescence.

Zhang L, Becker DF - Front Plant Sci (2015)

Potential linkages between proline metabolism and signaling pathways in petal and leaf senescence. Petal senescence (A): Aging induced petal senescence results in ROS accumulation and sugar depletion. SnRK1, activated in response to depleted sugar, is proposed to induce PRODH1/2 expression via bZIP1, bZIP11, and bZIP53. Upregulation of PRODH1/2 expression would be predicted to generate ATP thereby attenuating increases in ADP/ATP. PRODH activity is also expected to generate ROS as a by-product, possibly leading to activation of MPK20 and increased Mn-SOD activity. Enhanced Mn-SOD activity would help diminish accumulated ROS and oxidative damage during petal senescence. Activation of MAPK pathways by ROS would induce expression of antioxidant enzymes and petal abscission. Leaf senescence (B): Leaf senescence can be induced by plant hormones, age and detachment. During age-related senescence, the expression of PRODH2 and P5CDH are induced, suggesting a higher flux of proline catabolism and more glutamate available for nitrogen recycling. In response to H2O2 during hormone-induced senescence, PI3K may down-regulate PRODH1 resulting in less ROS signaling and adaptation to oxidative stress. Also during hormone-induced senescence, phospholipase D (PLD) and its product phosphatidic acid (PA) inhibit P5CS1 expression.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4544304&req=5

Figure 2: Potential linkages between proline metabolism and signaling pathways in petal and leaf senescence. Petal senescence (A): Aging induced petal senescence results in ROS accumulation and sugar depletion. SnRK1, activated in response to depleted sugar, is proposed to induce PRODH1/2 expression via bZIP1, bZIP11, and bZIP53. Upregulation of PRODH1/2 expression would be predicted to generate ATP thereby attenuating increases in ADP/ATP. PRODH activity is also expected to generate ROS as a by-product, possibly leading to activation of MPK20 and increased Mn-SOD activity. Enhanced Mn-SOD activity would help diminish accumulated ROS and oxidative damage during petal senescence. Activation of MAPK pathways by ROS would induce expression of antioxidant enzymes and petal abscission. Leaf senescence (B): Leaf senescence can be induced by plant hormones, age and detachment. During age-related senescence, the expression of PRODH2 and P5CDH are induced, suggesting a higher flux of proline catabolism and more glutamate available for nitrogen recycling. In response to H2O2 during hormone-induced senescence, PI3K may down-regulate PRODH1 resulting in less ROS signaling and adaptation to oxidative stress. Also during hormone-induced senescence, phospholipase D (PLD) and its product phosphatidic acid (PA) inhibit P5CS1 expression.
Mentions: The molecular pathways by which proline metabolism is regulated during plant senescence are summarized in Figure 2. The ability of proline to delay senescence in petal and leaf tissues is likely due to protection against oxidative stress that occurs in the aging tissue. In leaf, proline may help redistribute nitrogen to younger tissue whereas in flowers, proline helps counter energy shortages. Further insights into how proline metabolism impacts petal and leaf senescence will require additional studies that connect proline with plant senescence signaling pathways. Exploration of the linkages between proline metabolism and important pathways of plant senescence such as MAPK signaling, the SnRK1-bZIP pathway and PI3K signaling will be valuable targets for future study. Better understanding of proline metabolism in senescing leaves may uncover novel strategies for preserving post-harvest flowers and delaying stress-induced leaf senescence.

Bottom Line: Proline metabolism is manipulated under stress by multiple and complex regulatory pathways and can profoundly influence cell death and survival in microorganisms, plants, and animals.Though the effects of proline are mediated by diverse signaling pathways, a common theme appears to be the generation of reactive oxygen species (ROS) due to proline oxidation being coupled to the respiratory electron transport chain.Future studies focusing on the mechanisms by which proline metabolic shifts occur during senescence may lead to novel methods to rescue crops under stress and to preserve post-harvest agricultural products.

View Article: PubMed Central - PubMed

Affiliation: Redox Biology Center, Department of Biochemistry, University of Nebraska-Lincoln , Lincoln, NE, USA.

ABSTRACT
The amino acid proline has a unique biological role in stress adaptation. Proline metabolism is manipulated under stress by multiple and complex regulatory pathways and can profoundly influence cell death and survival in microorganisms, plants, and animals. Though the effects of proline are mediated by diverse signaling pathways, a common theme appears to be the generation of reactive oxygen species (ROS) due to proline oxidation being coupled to the respiratory electron transport chain. Considerable research has been devoted to understand how plants exploit proline metabolism in response to abiotic and biotic stress. Here, we review potential mechanisms by which proline metabolism influences plant senescence, namely in the petal and leaf. Recent studies of petal senescence suggest proline content is manipulated to meet energy demands of senescing cells. In the flower and leaf, proline metabolism may influence ROS signaling pathways that delay senescence progression. Future studies focusing on the mechanisms by which proline metabolic shifts occur during senescence may lead to novel methods to rescue crops under stress and to preserve post-harvest agricultural products.

No MeSH data available.


Related in: MedlinePlus