Ionizing　radiation　(IR)　is　a　common　therapeutic　agent　in　cancer　therapy.　It　damages　normal　tissue　and　causes　side　effects　including　dermatitis　and　mucositis.　Here　we　use　the　feather　follicle　as　a　model　to　investigate　the　mechanism　of　IR-induced　tissue　damage,　because　any　perturbation　of　feather　growth　will　be　clearly　recorded　in　its　regular　yet　complex　morphology.　We　find　that　IR　induces　defects　in　feather　formation　in　a　dose-dependent　manner.　No　abnormality　was　observed　at　5　Gy.　A　transient,　reversible　perturbation　of　feather　growth　was　induced　at　10　Gy,　leading　to　defects　in　the　feather　structure.　This　perturbation　became　irreversible　at　20　Gy.　Molecular　and　cellular　analysis　revealed　P53　activation,　DNA　damage　and　repair,　cell　cycle　arrest　and　apoptosis　in　the　pathobiology.　IR　also　induces　patterning　defects　in　feather　formation,　with　disrupted　branching　morphogenesis.　This　perturbation　is　mediated　by　cytokine　production　and　Stat1　activation,　as　manipulation　of　cytokine　levels　or　ectopic　Stat1　over-expression　also　led　to　irregular　feather　branching.　Furthermore,　AG-490,　a　chemical　inhibitor　of　Stat1　signaling,　can　partially　rescue　IR-induced　tissue　damage.　Our　results　suggest　that　the　feather　follicle　could　serve　as　a　useful　model　to　address　the　in　vivo　impact　of　the　many　mechanisms　of　IR-induced　tissue　damage.