Define leaf senescence. Describe important physiological and biochemical changes taking place during this process. Comment upon the regulation of senescence by phytohormones.

Defining Leaf Senescence

Leaf senescence is defined as the genetically controlled, developmentally regulated process leading to the systematic degradation of cellular components, ultimately resulting in leaf abscission. It is distinct from necrosis, which is caused by injury or stress and involves uncontrolled cell death. Senescence is an active process, requiring energy expenditure and the coordinated expression of numerous genes.

Physiological Changes During Leaf Senescence

Several key physiological changes characterize leaf senescence:

• Chlorophyll Degradation: This is one of the most visible signs of senescence. Chlorophyll is broken down by the enzyme chlorophyllase, leading to the unmasking of pre-existing carotenoids, resulting in yellow or orange coloration.
• Photosynthetic Capacity Decline: The efficiency of photosynthesis decreases as chlorophyll degrades and photosynthetic proteins are broken down.
• Reduced Water Potential: Senescing leaves often exhibit reduced water potential, contributing to their wilting appearance.
• Stomatal Closure: Stomata close, reducing gas exchange and further limiting photosynthetic activity.
• Nutrient Remobilization: A significant portion of nutrients, particularly nitrogen, phosphorus, and potassium, are remobilized from senescing leaves to other parts of the plant. This is a crucial aspect of senescence, ensuring efficient resource allocation.

Biochemical Changes During Leaf Senescence

The physiological changes are underpinned by a series of complex biochemical alterations:

• Protein Degradation: Proteins, including Rubisco (the key enzyme in carbon fixation), are broken down by proteases. The resulting amino acids are transported to sink tissues.
• Lipid Peroxidation: Membrane lipids undergo peroxidation, leading to membrane damage and loss of cellular integrity.
• Nucleic Acid Degradation: DNA and RNA are degraded, releasing nucleotides that can be remobilized.
• Increased Reactive Oxygen Species (ROS): ROS production increases during senescence, contributing to oxidative stress and cellular damage. However, ROS also act as signaling molecules in the senescence process.
• Accumulation of Senescence-Associated Genes (SAGs): The expression of specific genes, known as SAGs, is upregulated during senescence. These genes encode proteins involved in various aspects of the senescence process, such as protein degradation and nutrient remobilization.

Regulation of Senescence by Phytohormones

Phytohormones play a crucial role in regulating leaf senescence. Their effects are often complex and interconnected:

• Ethylene: Often considered the primary hormone promoting senescence. It stimulates chlorophyll degradation, protein breakdown, and abscission.
• Abscisic Acid (ABA): ABA promotes senescence, particularly under stress conditions like drought. It interacts with ethylene to accelerate the process.
• Auxin: Generally inhibits senescence. High auxin levels maintain leaf greenness and delay senescence. Declining auxin levels are often a trigger for senescence initiation.
• Cytokinins: Also inhibit senescence by delaying chlorophyll degradation and maintaining protein synthesis. Cytokinin levels often decline with age, contributing to senescence.
• Jasmonic Acid (JA): JA can promote senescence, particularly in response to wounding or pathogen attack.
• Salicylic Acid (SA): SA generally delays senescence, often acting antagonistically to JA.

Phytohormone	Effect on Senescence
Ethylene	Promotes
Abscisic Acid (ABA)	Promotes (especially under stress)
Auxin	Inhibits
Cytokinins	Inhibits
Jasmonic Acid (JA)	Promotes (in response to stress)
Salicylic Acid (SA)	Inhibits