Uteri from immature (21-day-old) and adult mice show different patterns of cell division in response to a physiological dose of 17β-estradiol. In the immature mouse uterus, estradiol increased stromal and epithelial cell proliferation by shortening the cell generation time (T_c). The epithelial T_c was reduced from 100 to 14.5 h; the stromal T_c was reduced to 16 h. In both cell types, the reduction in T_c was primarily due to a reduction of the G₁ phase of the cell cycle. In the adult mouse uterus, estradiol stimulated epithelial but not stromal cell proliferation. Here, estradiol reduced the epithelial T_c from 86 to 13 h, mostly by reducing the G₁ phase of the cell cycle. Therefore, estrogens stimulate uterine hyperplasia by selectively decreasing the G₁ phase of the cell cycle in specific cell populations. At some point during reproductive tract maturation, uterine stromal cells lose their ability to divide in response to estrogen stimulation. A developmental study showed that in the intact mouse, the stromal cell population gradually lost its ability to divide in response to estrogen stimulation during days 22–52 after birth. In prepubertally ovariectomized mice, the stromal cell population showed a very low mitotic response to estrogen stimulation at all ages. Thus, an ovarian mechanism may regulate the change in stromal responsiveness to estrogen stimulation. (Endocrinology114: 694, 1984)