Dynamic regulation of tissue fluidity controls skin repair during wound healing. During skin wound repair, the basal cell layer transitions from a solid-like homeostatic state to a fluid-like state that allows tissue remodeling during repair and then progressively returns to a solid-like state with re-epithelialization. Clonal analysis after cell ablation uncovers dynamic of skin SCs during tissue repair. Mathematical modeling supports a density-dependent promotion of symmetric SC division. Wound healing involves dynamic changes in tissue fluidity. EGFR/AP1 axis controls a regenerative state that regulates tissue fluidity and repair. In this study, the authors developed a mouse model allowing lineage tracing and basal cell lineage ablation to monitor SC fate and tissue dynamics during regeneration using confocal and intravital imaging. Analysis of basal cell rearrangements shows dynamic transitions from a solid-like homeostatic state to a fluid-like state allowing tissue remodeling during repair, as predicted by a minimal mathematical modeling of the spatiotemporal dynamics and fate behavior of basal cells. The basal cell layer progressively returns to a solid-like state with re-epithelialization. Bulk, single-cell RNA, and epigenetic profiling of SCs, together with functional experiments, uncover a common regenerative state regulated by the EGFR/AP1 axis activated during tissue fluidization that is essential for skin SC activation and tissue repair. The study reveals that tissue repair occurs rapidly following the depletion of more than 50% of the basal cell population of the IFE. This depletion induces a transient burst of cell proliferation in the IFE and infundibulum and a switch from population asymmetric renewal to an increase in duplicative (self-renewing) divisions. Despite the absence of depletion of the suprabasal differentiated cells, the replenishment of basal cells is accompanied by an increase in the production of differentiated cells, showing that renewing divisions are tightly coupled with epidermal differentiation. The study also shows that tissue fluidization during repair ensures that the basal cell layer can remodel and reset the tissue structure and architecture. Once re-established, the basal cell layer recovers the solid-like homeostatic state to restore skin barrier function. Transitions between fluid-like and solid-like tissue states have been reported in many biological contexts, including embryonic development and tumor progression. Our results indicate that regulated tissue fluidization is also required during the initial stage of tissue repair in mice skin. Tissue fluidization, caused by decreased tissue contractility, is believed to facilitate wound closure in epithelial monolayers. We find the opposite behavior in mammalian skin repair, with decreased tissue contractility rigidifying the tissue and slowing down regeneration, suggesting that a different fluidization mechanism is involved in skin regeneration. The study identifies a dynamic regulation of tissue fluidity during wound healing that is essential for tissue repair and uncovers a common regenerative cell state across different epidermal SCs that is regulated by the EGFR/MEK/AP1 signalingDynamic regulation of tissue fluidity controls skin repair during wound healing. During skin wound repair, the basal cell layer transitions from a solid-like homeostatic state to a fluid-like state that allows tissue remodeling during repair and then progressively returns to a solid-like state with re-epithelialization. Clonal analysis after cell ablation uncovers dynamic of skin SCs during tissue repair. Mathematical modeling supports a density-dependent promotion of symmetric SC division. Wound healing involves dynamic changes in tissue fluidity. EGFR/AP1 axis controls a regenerative state that regulates tissue fluidity and repair. In this study, the authors developed a mouse model allowing lineage tracing and basal cell lineage ablation to monitor SC fate and tissue dynamics during regeneration using confocal and intravital imaging. Analysis of basal cell rearrangements shows dynamic transitions from a solid-like homeostatic state to a fluid-like state allowing tissue remodeling during repair, as predicted by a minimal mathematical modeling of the spatiotemporal dynamics and fate behavior of basal cells. The basal cell layer progressively returns to a solid-like state with re-epithelialization. Bulk, single-cell RNA, and epigenetic profiling of SCs, together with functional experiments, uncover a common regenerative state regulated by the EGFR/AP1 axis activated during tissue fluidization that is essential for skin SC activation and tissue repair. The study reveals that tissue repair occurs rapidly following the depletion of more than 50% of the basal cell population of the IFE. This depletion induces a transient burst of cell proliferation in the IFE and infundibulum and a switch from population asymmetric renewal to an increase in duplicative (self-renewing) divisions. Despite the absence of depletion of the suprabasal differentiated cells, the replenishment of basal cells is accompanied by an increase in the production of differentiated cells, showing that renewing divisions are tightly coupled with epidermal differentiation. The study also shows that tissue fluidization during repair ensures that the basal cell layer can remodel and reset the tissue structure and architecture. Once re-established, the basal cell layer recovers the solid-like homeostatic state to restore skin barrier function. Transitions between fluid-like and solid-like tissue states have been reported in many biological contexts, including embryonic development and tumor progression. Our results indicate that regulated tissue fluidization is also required during the initial stage of tissue repair in mice skin. Tissue fluidization, caused by decreased tissue contractility, is believed to facilitate wound closure in epithelial monolayers. We find the opposite behavior in mammalian skin repair, with decreased tissue contractility rigidifying the tissue and slowing down regeneration, suggesting that a different fluidization mechanism is involved in skin regeneration. The study identifies a dynamic regulation of tissue fluidity during wound healing that is essential for tissue repair and uncovers a common regenerative cell state across different epidermal SCs that is regulated by the EGFR/MEK/AP1 signaling