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Germ Cells and Somatic Cells Follow ‘Different Rules’ for Programmed Cell Death
Published in Cell Death Differ., the study reveals distinct mechanisms governing programmed cell death in somatic and germ cells of C. elegans.
Programmed cell death is a biological process in which cells die according to predetermined rules, removing unnecessary cells during development and safely eliminating damaged cells. When programmed cell death does not occur properly, cells between the developing fingers may remain, causing the fingers to remain joined together, while defective cells may continue to proliferate and develop into cancer. A new study has found that the rules governing programmed cell death differ depending on the type of cell.
A research team led by Professor Anton Gartner of the UNIST Graduate School of Health Science and Technology, in collaboration with a team led by Research Fellow Nadin Memar at the Institute for Basic Science (IBS) Center for Genomic Integrity, has identified different mechanisms that determine the programmed cell death in embryonic somatic cells and adult germ cells of Caenorhabditis elegans .
According to the study, the signal that initiates programmed cell death was activated only in embryonic somatic cells destined to die. In germ cells, however, a 'two-step regulatory system' separated the activation of the death signal in response to DNA damage from the actual execution of cell death. When the researchers induced DNA damage using radiation, the cell death-initiating gene egl-1 was activated throughout the germline, but only a subset of germ cells in the late pachytene stage—when chromosomes are inspected before the cells develop into eggs—actually died.
The researchers interpreted this two-step regulation as a safeguard that may help prevent the organism from losing all of its germ cells, which are essential for reproduction and species survival, while still eliminating severely damaged cells. Germ cells broadly prepare for death in response to damage signals, but only those at a particular developmental stage and meeting additional conditions proceed to die. This mechanism may allow the organism to preserve enough germ cells for reproduction while reducing the risk that damaged genetic information is passed on to the next generation.
The researchers noted that further studies are needed to identify the specific downstream mechanisms that determine why only some germ cells ultimately undergo cell death.
The team uncovered these findings by using gene-editing technology to attach fluorescent markers to four programmed cell death genes and their associated proteins. C. elegans is particularly well suited for tracking cell death because its body is transparent, it has only 959 somatic cells as an adult, and the birth and death of every cell—including the 131 cells eliminated during development—have been mapped in detail.

Fluorescence imaging further showed that cell death-regulating proteins such as CED-4 and CED-3 change their cellular localization according to tissue type and developmental stage. This supports the researchers' hypothesis that programmed cell death is not controlled simply by switching genes on and off, but through a highly coordinated regulatory process that also involves dynamic changes in protein localization.
The research team added, “Because gene families similar to the major programmed cell death genes in C. elegans are conserved in humans and other mammals, these findings could provide fundamental information for understanding diseases such as cancer, in which the regulation of programmed cell death is disrupted.”
The team added, “The fluorescent imaging tools developed in this study could be used to investigate the conditions under which cells die or survive in model organisms.”
This work was supported by the Institute for Basic Science (IBS) and by grants from the National Research Foundation of Korea (NRF), funded by the Ministry of Science and ICT. The findings were published online in Cell Death & Differentiation on June 10, 2026.
Anton Gartner
Professor, Graduate School of Health Science and Technology, UNIST
IBS Center for Genomic Integrity (CGI)
E: tgartner@unist.ac.kr
William I. Suh
IBS Public Relations Team
E: willisuh@ibs.re.kr
Notes for Editors
The online version of the original article can be found HERE .
Journal Reference
Gokul Gopakumar, Afroza Aman, Stéphane GM Rolland, et al., "Endogenous expression and subcellular localization of core apoptosis regulators reveal key differences between embryonic and germline apoptosis in C. elegans," Cell Death Differ., (2026).
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