Leaf Senescence is one of the most significant changes during autumn. It describes a natural event that occurs during this season. Many people often recognize the autumn color of leaves. This event happens because of programmed cell death that in the plant. Needless to say, plants exist because of the co-existence of cells. Therefore, the occurrence and survival of a leaf is because of the normal and proper functioning of cells. The field of apoptosis is expanding at a rapid rate.
Leaf Senescence usually signifies the aging process in plants. There is a decrease in the metabolic processes in a plant. Moreover, the color change is due to the breakdown of chloroplasts. Leaf senescence manifests increases the fragility of the leaf. In fact, it leads to an increase in membrane fragility. Undoubtedly, the process of leaf senescence occurs as a result of apoptosis. Apoptosis refers to the natural and programmed cell death that occurs in living things. It is a crucial process that is essential for survival. (Besseauet. Al. 56).
Senescence occurs in the various sections and levels of the plant. They are many assays that can help detect the process of apoptosis in organisms. This reports helps summarize the consequences of apoptosis as it expresses itself in leaf senescence. Apoptosis is a process that uses a complex initiation process. There are apoptotic signals that promote apoptosis. Any factors of stress, hypoxia, external trauma, and trauma always activate apoptosis. Additionally, the mitochondria plays a crucial role in regulating this process. It releases caspases that may activate apoptosis regulation. The Fas pathway is also a regulator of apoptosis. The goal of this review is to elaborate the intracellular and extracellular changes that occur during leaf senescence.
Apoptotic Changes That Occur During Leaf Senescence.
Leaf senescence is usually signaled by a series of transcription factors. The NAC transcription factors take part in the sequencing pattern. The N-terminal factors have DNA binding domains that regulate the process of senescence. Moreover, the WRKY has a finger-like motif that ensures DNA is bound. These transcription factors also take part in leaf senescence. This change has a lot of significance because it leads to the characteristic leaf drooping. Senescence is a form of apoptosis because it leads to programmed cell death. There are a lot of evidences that make this hypothesis true.
Leaf senescence involves the breakdown of macromolecules including starch, nucleic acid and cellulose. It is the reason why many plants wither during this period. There are internal and external factors of leaf senescence. The internal factors include the function of hormones. These hormones include cytokinin, auxin, and ethylene. These hormones a crucial role in regulating the process of leaf senescence. There is also a form of cellular shrinkage that occurs sometime after autolysis. It happens because of the irreversible loss of cellular components in the cytoplasm.
The loss of the cellular wall and membrane also takes place during leaf senescence. External factors of leaf senescence include the presence of drought, oxidative stress, and pathogen attack. These elements may contribute to the initiation of leaf senescence. Pathogen attack causes the withering of leaves and loss of the green color. It is mediated by the WRKY30 gene. It takes a while for a plant to deplete starch; which is a complex compound that has successive glucose elements. ATP usually supports the Na+/K+-ATPase component in the cellular membrane cells (Besseauet. Al. 88).
There are various factors that take part in the regulation of leaf senescence. Chromatin-mediated regulation involves the use of the ORE7 and HDA6 genes. They ensure that this process takes place in a controlled manner. Post-transcriptional regulation involves the use the miR164 gene. The translational gene regulator is the ORE4. As mentioned earlier, the transcriptional regulators are many. They include ARF2, NAP, WRKY, JUB1 and RAV1. The posttranslational gene regulators include the ORE9. Therefore, it is vivid to say that the initial signal originates from the transcriptional processes in the nucleus (Fukaoet. Al. 235).
Many cellular processes always occur in the mitochondria. Light and microscopic examination of the mitochondria during apoptosis shows very dynamic changes. The mitochondria are the main energy generators. They have cytosolic enzymes that participate in the Emden Meyerhof and the Hexose monophosphate pathways. Each mitochondrion has a folded matrix. It has a large surface area to volume ratio that supports various enzymatic reactions.
Research shows that there is release of a chemical messenger from the mitochondrion before apoptosis. This chemical is cytochrome c. Studies suggest that cytochrome c is the main transmitter in the apoptotic process. The mitochondrion has a double membrane, the inner membrane forms cristae. Consequently, the cristae take part in the synthesis of cytochrome cells (Besseauet. Al. 76).
Cytochrome c is bound to the inner membrane by cardiolipin which is a charged lipid. There are weak covalent bonds that promote the formation of this bond. During apoptosis, research shows that there is subsequent breakage of this weak attraction. It is evident that the release of cytochrome c precedes the formation of autophagolysosomes in the cytoplasm. My research showed that there exists a protein that regulates the release of cytochrome c. Needless to say; this regulation prevents both extremes of apoptosis.
Leaf senescence always differs with age. In fact, there is a marked increase in reactive oxygen species during the aging processes. Also, lipid peroxidation is a marker of cellular aging. Alternatively, lack of apoptosis in cells predisposes an organism to excessive proliferation. Opa1 is a transmembrane protein that promotes the bond between cytochrome c and cardiolipin. Often, the signal of apoptosis is the intracytoplasmic influx of calcium ions. These calcium ions subsequently enter the mitochondrial matrix.
They lead to an instant response in the cristae. The attenuation of the bond between cardiolipin and cytochrome c leads to the progressive release of cytochrome c. Pores in the membrane promote the efflux into the cytoplasm. Consequently, cytochrome c activates the lysosomes. The lysosomes start releasing autolytic enzymes into cellular components. It is a significant feature of irreversible cellular death (Penfold & Vicky, 232).
Electron microscopy always portrays a diverse array changes that occur in the mitochondria. One significant change always affects the matrix. Cessation of mitochondrial functions leads to the blebbing of the matrix. The formation of complexes and accumulation of granules leads to this observation. Additionally, mitochondrial swelling is a characteristic of irreversible cellular death. The swelling is a result of influx of water and electrolytes to the hypotonic interior of the mitochondria.
The influx happens because of the dysfunction of the sodium-potassium pump due to the presence of depleted energy. Another morphological change takes place in the cristae. Scientists refer to this phenomenon as cristae remodeling. The cristae are always tubular in structure. During apoptosis, they become loose, round fragments. Consequently, these fragments disappear. A mitochondrion always loses the ability to function properly after this phenomenon.
Consequently, the mitochondrion loses its filamentous structure and becomes fragmented. This transformation is similar to the fragmentation of the nucleus. Scholars refer to it as karyorhexis. It usually accompanies karyolysis and pyknosis. Pyknosis refers to the subsequent decrease in size of the nucleus during apoptosis. It elaborates the condensation of the nucleus in cells. Moreover, karyolysis refers to the complete dissolution of the nuclear chromatin. These changes always take place gradually during apoptosis (Penfold& Vicky, 301).
Many experts have extensively studied apoptosis. Their results show that chloroplasts have a minor role in the apoptotic process. In fact, previous research showed that the chloroplasts do not take part in apoptosis. However, scientists decided to carry out a laboratory test. The test required the presence of illumination, pea leaves and cyanide. Needless to say, a leaf contains both chemotropic and phototrophic cells. An epidermal peel would provide a suitable monolayer of cells that had both cell types.