Plants are sessile organisms that cannot escape environmental hazards, which induce DNA damage and produce mutations. Plants are also subject to DNA damage caused by cellular processes such as transposon movement. Plant stem cells in particular must be protected from genotoxicity as they are the origin of all organs, together with the germline. In accordance with this premise, plant stem cells were found to be hypersensitive to Double Strand Breaks (DSBs), leading to their specific killing via the Ataxia Telangiectasia Mutated (ATM) and Suppressor of Gamma Response 1 (SOG1) genes, showing that plant stem cells developed a specific protection mechanism against genotoxicity. However, the components of the pathway leading to programmed cell death (PCD) are still unknown, and the in vivo DNA damaging agents responsible for this mechanism have not been characterized, forming the basis of this project. A candidate gene approach together with a forward genetics screen in the root stem cells did not yield new factors of the ATM/SOG1 pathway. However, a specific ecotype showed an absence of DSBs-induced PCD, hinting at the existence of natural variation in stem cell responses to DSBs. Then, we tested the hypothesis that endogenous DNA damage could be the trigger for stem cell hypersensitivity to DNA damage. We first uncovered an unexpected link between the DNA damage response pathway and chromatin silencing by characterizing the silencing of a transgene following a recombination event in the shoot stem cells. This silencing was dependent on ATM/SOG1 and linked to the production of 24-nt siRNA and RNA polymerase IV and argonaute 6 (AGO6). We then identified several chromatin silencing mutants showing spontaneous PCD in the root stem cells, and studied the link between transposon silencing and the ATM/SOG1 pathway. This thesis provides a link between DNA damage responses and chromatin silencing in Arabidopsis stem cells.