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Apoptosis Induced Proliferation as a Phenomenon

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An important element of apoptosis induced by stress is that there is a substantial number of cell deaths even for lower doses of radiation. Studies have anticipated for more that 50% of cell to enter apoptosis after a large radiation dose (Haynie and Bryant, 1977). As stated earlier, the stem cell niche of the Drosophila testis has the extraordinary ability to restore its GSCs even after losing them all (de Cuevas and Matunis., 2011). This suggests the existence of a phenomenon called apoptosis induced proliferation. This phenomenon indicates that surviving cells undergo additional proliferation after a stress-induced event to regenerate and compensate for lost cells. This would also suggest that the occurrence of the stress event that results in the substantial cell deaths, can also produce a stimulus which induces proliferation (Martin, Perez-Garijo and Morata, 2009).

It has been observed in a range of studies that apoptotic cells help in stimulating regeneration of tissue by secreting mitogens (chemical substance promotes cells to initiate cell division and activating mitosis) that induce proliferation in adjacent cells. (Pahwa, Good and Hoffmann, 1981; Steller, 2008). Dmp53 and the caspase Dronc are required in apoptosis-induced proliferation alongside the secretion of mitogens such as Decapentaplegic (Dpp) and Wingless (Wg) (Dichtel-Danjoy et al., 2012). Research has found that mutated Dronc suppress apoptosis induced proliferation that is induced by the pro-apoptotic proteins or irradiation. It has also been shown that there is a link between Dmp53 and Dronc; Dmp53 is essential for the activation of apoptosis induced proliferation and is transcriptionally initiated by cells that are ‘undead’ by a process that entails the function of Dronc (Steller.,2008)

Subsequently, signalling pathways including Notch and Jak/STAT have been associated with the activation of proliferation induced by apoptosis (Stella., 2008). For instance, in drosophila the vacuolar protein sorting genes vps23 and vps25 function throughout the sorting of endosomal proteins, to inactivate cell surface receptors. It has been found that mutations of these genes cause non-autonomous tissue growth and independently induce apoptosis. Consequently, vps23 and vps25 being unable to function would result in defects of the endosome, which would lead to accumulation at the endosome of cell-surface receptors. The receptors which is predominantly sensitive to disturbances in the endosome is the Notch receptor. The accumulation of cell-surface receptors at the endosome results in unsuitable notch activity. This then leads to secretion of molecules similar to interleukin-6, that activate the signalling pathway Jak/STAT in adjacent cells and subsequently apoptosis induced proliferation (Fan and Bergmann., 2008)

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Apoptosis Induced Proliferation as a Phenomenon. (2018, November 15). GradesFixer. Retrieved May 23, 2022, from
“Apoptosis Induced Proliferation as a Phenomenon.” GradesFixer, 15 Nov. 2018,
Apoptosis Induced Proliferation as a Phenomenon. [online]. Available at: <> [Accessed 23 May 2022].
Apoptosis Induced Proliferation as a Phenomenon [Internet]. GradesFixer. 2018 Nov 15 [cited 2022 May 23]. Available from:
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