"You have made your way from worm to man, and much within you is still a worm" - "당신은 벌레에서 사람으로 길을 갔고, 당신 안에는 여전히 벌레다" (Nieztsche)
This section is led by Anton Gartner, uses C. elegans as a simple animal model to study pathways leading to DNA damage dependent apoptosis induction in the germline. This section also studies the transcriptional responses resulting from the exposure to ionizing irradiation, focusing on p53 and oxidative stress signaling.
Apoptosis is essential to eliminate damaged cells, and its deficiency is associated with cancer. Apoptosis is particularly important in germ cells, eliminating the majority of them. The Gartner lab in the past worked out the p53 (C. elegans CEP-1) dependent germ cell apoptosis pathway. A key protein for apoptosis regulation is the conserved CED-9 (C. elegans)/ Bcl2 (human) protein that protects cells from undergoing apoptosis. However, it is still not fully understood how Bcl2 proteins trigger mitochondrial permeabilization and Apaf1 (C. elegans CED-4) mediated activation of caspases triggering apoptosis in response to DNA damage. We strive to better understand the function of CED-9, CED-4, and EGL-1 during DNA damage-induced apoptosis. EGL-1 and CED-13 are conserved pro-apoptotic BH3-only domain proteins that act by binding to and inhibiting CED-9/Bcl2. During development egl-1 cell type-specific transcriptional induction precedes apoptosis and is necessary for apoptosis induction. We have previously shown that ionizing radiation (IR) leads to the CEP-1 dependent EGL-1 and CED-13 induction in the germ line. Interestingly, we also found that genes not related to known apoptosis and repair genes are induced by IR independent of CEP-1. It is likely that this transcriptional response is linked to oxidative stress and part of an organismal defense mechanism where DNA damage responses and organismal stress responses are coordinated.