Although 17-estradiol (E2) is recognized as a potent hair growth modulator, our knowledge of estrogen function, signaling and target genes in hair biology is still very limited. Among the two recognized estrogen receptors, (ER, ER), only ER had been detected in murine skin. Here, we show that ER, ER and ERins are all expressed throughout the murine hair cycle, both at the protein and the RNA level, but show distinct expression patterns. We confirm that topical 17 estradiol (E2) arrests murine pelage hair follicles in telogen, and demonstrate that E2 is a potent inducer of premature catagen development. The ER antagonist ICI 182.780 does not induce anagen initiation, but accelerates anagen development and wave spreading in female mice. ER knock-out mice displayed accelerated catagen development, along with an increase in the number of apoptotic hair follicle keratinocytes. This suggests that contrary to previous concepts, ER does indeed play a significant role in murine hair growth control: while the catagen-promoting properties of E2 are mediated via ER, ER mainly may function as a silencer of ER action in hair biology. These findings illustrate the complexity of hair growth modulation by estrogens, and suggest that one key to more effective hair growth manipulation with ER ligands lies in the use of selective ER or - antagonists/agonists. Our study also underscores that the hair cycling response to estrogensoffers an ideal model for studying the controls and dynamics of wave propagation in biological systems.