Programmed cell death
Programmed cell death (PCD; sometimes referred to as cellular suicide tissue development.
Apoptosis and autophagy are both forms of programmed cell death.[4] Necrosis is the death of a cell caused by external factors such as trauma or infection and occurs in several different forms. Necrosis was long seen as a non-physiological process that occurs as a result of infection or injury,[4] but in the 2000s, a form of programmed necrosis, called necroptosis,[5] was recognized as an alternative form of programmed cell death. It is hypothesized that necroptosis can serve as a cell-death backup to apoptosis when the apoptosis signaling is blocked by endogenous or exogenous factors such as viruses or mutations. Most recently, other types of regulated necrosis have been discovered as well, which share several signaling events with necroptosis and apoptosis.[6]
History
The concept of "programmed cell-death" was used by Lockshin & Williams[7] in 1964 in relation to insect tissue development, around eight years before "apoptosis" was coined. The term PCD has, however, been a source of confusion and Durand and Ramsey[8] have developed the concept by providing mechanistic and evolutionary definitions. PCD has become the general terms that refers to all the different types of cell death that have a genetic component.
The first insight into the mechanism came from studying
PCD has been the subject of increasing attention and research efforts. This trend has been highlighted with the award of the 2002
Types
- Apoptosis or Type I cell-death.
Apoptosis
Autophagy
Mechanism
A critical regulator of autophagy induction is the
The
Other types
Besides the above two types of PCD, other pathways have been discovered.[14] Called "non-apoptotic programmed cell-death" (or "caspase-independent programmed cell-death" or "necroptosis"), these alternative routes to death are as efficient as apoptosis and can function as either backup mechanisms or the main type of PCD.
Other forms of programmed cell death include
Aponecrosis is a hybrid of apoptosis and necrosis and refers to an incomplete apoptotic process that is completed by necrosis.[18]
Pyroptosis, an inflammatory type of cell death, is uniquely mediated by caspase 1, an enzyme not involved in apoptosis, in response to infection by certain microorganisms.[20]
Plant cells undergo particular processes of PCD similar to autophagic cell death. However, some common features of PCD are highly conserved in both plants and metazoa.
Atrophic factors
An atrophic factor is a force that causes a cell to die. Only natural forces on the cell are considered to be atrophic factors, whereas, for example, agents of mechanical or chemical abuse or lysis of the cell are considered not to be atrophic factors.[by whom?] Common types of atrophic factors are:[21]
- Decreased workload
- Loss of innervation
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrinestimulation
- Senility
- Compression
Role in the development of the nervous system
The initial expansion of the developing
Role in neural development
PCD in the developing nervous system has been observed in proliferating as well as post-mitotic cells.
The neurotrophic theory
The neurotrophic theory is the leading hypothesis used to explain the role of programmed cell death in the developing nervous system.[29] It postulates that in order to ensure optimal innervation of targets, a surplus of neurons is first produced which then compete for limited quantities of protective neurotrophic factors and only a fraction survive while others die by programmed cell death.[26] Furthermore, the theory states that predetermined factors regulate the amount of neurons that survive and the size of the innervating neuronal population directly correlates to the influence of their target field.[30]
The underlying idea that target cells secrete attractive or inducing factors and that their
Peripheral versus central nervous system
Different mechanisms regulate PCD in the
Programmed cell death in the CNS is not dependent on external
Nervous system development in its absence
Programmed cell death can be reduced or eliminated in the developing nervous system by the targeted deletion of pro-apoptotic genes or by the overexpression of anti-apoptotic genes. The absence or reduction of PCD can cause serious anatomical malformations but can also result in minimal consequences depending on the gene targeted, neuronal population, and stage of development.
Invertebrates and vertebrates
Learning about PCD in various species is essential in understanding the evolutionary basis and reason for apoptosis in development of the nervous system. During the development of the
In contrast to invertebrates, the mechanism of programmed cell death is found to be more conserved in
In plant tissue
Programmed cell death in plants has a number of molecular similarities to animal apoptosis, but it also has differences, the most obvious being the presence of a cell wall and the lack of an immune system that removes the pieces of the dead cell. Instead of an immune response, the dying cell synthesizes substances to break itself down and places them in a vacuole that ruptures as the cell dies.[60]
In "APL regulates vascular tissue identity in
Basic morphological and biochemical features of PCD have been conserved in both plant and animal kingdoms.[62] Specific types of plant cells carry out unique cell-death programs. These have common features with animal apoptosis—for instance, nuclear DNA degradation—but they also have their own peculiarities, such as nuclear degradation triggered by the collapse of the vacuole in tracheary elements of the xylem.[63]
Janneke Balk and Christopher J. Leaver, of the Department of
PCD in pollen prevents inbreeding
During
In slime molds
The social
The stalk is composed of dead cells that have undergone a type of PCD that shares many features of an autophagic cell-death: massive vacuoles forming inside cells, a degree of chromatin condensation, but no DNA fragmentation.[67] The structural role of the residues left by the dead cells is reminiscent of the products of PCD in plant tissue.
D. discoideum is a slime mold, part of a branch that might have emerged from
Evolutionary origin of mitochondrial apoptosis
The occurrence of programmed cell death in protists is possible,[69][70] but it remains controversial. Some categorize death in those organisms as unregulated apoptosis-like cell death.[71][72]
Biologists had long suspected that
This evolutionary step would have been risky for the primitive eukaryotic cells, which began to engulf the energy-producing bacteria, as well as a perilous step for the ancestors of mitochondria, which began to invade their proto-eukaryotic hosts. This process is still evident today, between human white blood cells and bacteria. Most of the time, invading bacteria are destroyed by the white blood cells; however, it is not uncommon for the chemical warfare waged by prokaryotes to succeed, with the consequence known as infection by its resulting damage.
One of these rare evolutionary events, about
Mitochondriate eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules that can trigger cell suicide.[75] It is not clear why apoptotic machinery is maintained in the extant unicellular organisms. This process has now been evolved to happen only when programmed.[76] to cells (such as feedback from neighbors, stress or DNA damage), mitochondria release caspase activators that trigger the cell-death-inducing biochemical cascade. As such, the cell suicide mechanism is now crucial to all of our lives.
DNA damage and apoptosis
Repair of DNA damages and apoptosis are two enzymatic processes essential for maintaining genome integrity in humans. Cells that are deficient in DNA repair tend to accumulate DNA damages, and when such cells are also defective in apoptosis they tend to survive even with excess DNA damage[77]. Replication of DNA in such cells leads to mutations and these mutations may cause cancer (see Figure). Several enzymatic pathways have evolved for repairing different kinds of DNA damage, and it has been found that in five well studied DNA repair pathways particular enzymes have a dual role, where one role is to participate in repair of a specific class of damages and the second role is to induce apoptosis if the level of such DNA damage is beyond the cell’s repair capability[77]. These dual role proteins tend to protect against development of cancer. Proteins that function in such a dual role for each repair process are: (1) DNA mismatch repair, MSH2, MSH6, MLH1 and PMS2; (2) base excision repair, APEX1 (REF1/APE), poly(ADP-ribose) polymerase (PARP); (3) nucleotide excision repair, XPB, XPD (ERCC2), p53, p33(ING1b); (4) non-homologous end joining, the catalytic subunit of DNA-PK; (5) homologous recombinational repair, BRCA1, ATM, ATR, WRN, BLM, Tip60, p53.
Programmed death of entire organisms
Clinical significance
ABL
The BCR-ABL oncogene has been found to be involved in the development of cancer in humans.[78]
c-Myc
Metastasis
A
See also
- Anoikis
- Apoptosis-inducing factor
- Apoptosis versus Pseudoapoptosis
- Apoptosome
- Apoptotic DNA fragmentation
- Autolysis (biology)
- Autophagy
- Autoschizis
- Bcl-2
- BH3 interacting domain death agonist(BID)
- Calpains
- Caspases
- Cell damage
- Cornification
- Cytochrome c
- Cytotoxicity
- Diablo homolog
- Entosis
- Excitotoxicity
- Ferroptosis
- Inflammasome
- Mitochondrial permeability transition pore
- Mitotic catastrophe
- Necrobiology
- Necroptosis
- Necrosis
- p53 upregulated modulator of apoptosis (PUMA)
- Paraptosis
- Parthanatos
- Pyroptosis
- RIP kinases
- Wallerian degeneration
Notes and references
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