A multicellular organism’s cells are part of a well-organised community. The cells associated with this community are closely controlled—not just by controlling cell division rates but also by controlling cell death rates. When cells are no longer needed, they activate an intracellular death pathway and commit suicide. This is known as programmed cell death; however, it is more frequently referred to as apoptosis.
Programmed Cell Death
Programmed cell death is defined by definite external traits as well as energy-dependent molecular pathways. Apoptosis is thought to be important in a variety of activities, including normal cell turnover, immune system development and function, hormone-dependent atrophy, embryonic development, and chemical-induced cell death.
Apoptosis that is either too little or too much is a factor in a variety of human diseases, including neurodegenerative diseases, ischemia damage, autoimmune disorders, and cancer. The power to control whether a cell lives or dies is recognised for its enormous therapeutic potential. As a result, scientists are still working to understand and analyse the cell cycle machinery and signalling networks that control cell cycle arrest and apoptosis. To that goal, the field of apoptosis has been developed at a successive rate.
In developing and adult animal tissues, the amount of apoptosis that happens can be astounding. In the growing nervous system of vertebrates, for example, up to 50% or more of the nerve cells die soon after formation. Every hour, billions of cells die in the bone marrow and intestine of a healthy adult individual. It seems incredibly wasteful for so many cells to perish, especially considering that the vast majority of them are fully healthy at the moment of death.
What is the Aim of this Huge Cell Death?
In some circumstances, the solutions are obvious. Cell death during embryonic development sculpts mouse paws, as they start out as spadelike formations, and only when the cells between them are dead do the single digits separately. Cells also perish when the structure they create is no longer needed.
When a tadpole transforms into a frog, the cells in the tail die, and the frog’s tail, which is no longer needed, vanishes. In many other situations, cell death aids in the control of cell numbers.
Cell death, for example, changes the number of nerve cells in the developing nervous system to match the number of target cells that require innervation. Programmed cell death is the process through which cells die in all of these circumstances.
Cell death and cell division are perfectly balanced in adult tissues. If this were not the case, the tissue would expand or contract. In an adult rat, for example, when a portion of the liver is removed, liver cell proliferation rises to compensate for the loss.
In contrast, if a rat is given the medicine phenobarbital, which stimulates liver cell proliferation (and hence liver enlargement), and then the drug is removed, apoptosis in the liver skyrockets until the liver shrinks back to its previous size, generally within a week. As a result, the liver is preserved at a consistent size by controlling both cell death and cell birth rates.
Mechanism of Programmed Cell Death
Apoptosis has a complex and sophisticated mechanism involving an energy-dependent cascade of molecular reactions.
There are two main apoptotic mechanisms, according to research: the extrinsic or death receptor pathway and the intrinsic or mitochondrial pathway . There is also a route involving T-cell mediated cytotoxicity and performing granzyme-dependent cell death.
Granzyme B or granzyme A can both trigger apoptosis via the perforin/granzyme pathway. Extrinsic, intrinsic, and granzyme B routes all lead to the same execution pathway or terminal.
The cleavage of caspase-3 initiates this process, which culminates in DNA fragmentation and cytoskeleton destruction, cross-linking of proteins, creation of apoptotic bodies, production of ligands for phagocytic cell receptors, and eventually, absorption by phagocytic cells are all steps in the process.
The granzyme is a type of enzyme. Through single-stranded DNA damage, a pathway initiates parallel, caspase-independent cell death.
Programmed Cell Death in Plants and Animals
Apoptosis, autophagy, and necrosis are the three main kinds of programmed cell death (PCD) now recognised in mammals. These PCD classifications are based on cell shape rather than biochemical characteristics. Plants have even less knowledge of the biochemistry behind PCD than mammals; hence it appears that plant PCD classes must be identified mostly based on cell shape.
In Plants
The two primary plant programmed cell death types, as defined here, will be briefly detailed, followed by a description of the three basic animal PCD categories. Following that, an attempt will be made to describe the relationship between these plant PCD classes and animal PCD categories.
In Animals
Programmed cell death is a type of cell death characterised by cell rounding, cellular volume reduction, chromatin condensation, nuclear fragmentation, little or no ultrastructural modifications of cytoplasmic organelles, the production of large cell protrusions on the surface or fragmentation of the cell, and engulfment of these protrusions or apoptotic bodies by mobile phagocytes or neighbouring cells. As a result, the cell’s decomposition happens in another cell. The creation of cell protrusions or apoptotic bodies, as well as their elimination by other cells after phagocytosis, are the primary distinguishing aspects.
Examples of PCD in Animals and Plants
Apoptotic: Animals have a lot of it, but there aren’t any examples of it in plants.
Autophagic: It’s only linked to autophagic morphology.
There are numerous in animal cells.
Plants with an ‘Autolytic’ PCD:
In plants, below are a few examples of ‘non-autolytic’ PCD.
Death necessitates the presence of genes.
Only two specimens of animals are known to date: Caenorhabditis elegans and Drosophila Only two examples in plants have been identified to date: tracheary elements and certain HR-related PCDg.
Necrotic: In animal cells, it’s everywhere. The majority of ‘non-autolytic’ PCD cases in plant cells.
Conclusion
The genetic and molecular analysis of genes that affect developmental cell death in C. elegans when mutated or inactivated by RNAi has revealed some of the molecular pathways involved in the specification, killing, or execution phase of programmed cell death.