(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.

Fig. 6. 35S-in situ hybridization analysis of Foxl2,
activin-ßA, activin-ßB, follistatin, inhibin-
, Amh
(anti-Mullerian inhibiting hormone), Gdf9 and Kitl, at
different stages of ovary organogenesis (P, postnatal day; w, weeks). (A)
Foxl2 is expressed in granulosa cells at early stages of
folliculogenesis, whereas its expression declines to low levels in adult
mutant ovaries. (B) In 2-week-old ovaries activin-ßA is localized to
granulosa cells of antral follicles, whereas it is absent in
Foxl2-deficient ovaries. (C) In contrast, activin-ßB expression
is unaltered in mutant ovaries compared with WT ovaries. (D) Expression of
follistatin was significantly downregulated in
Foxl2lacZ homozygous mutant ovaries after P1. (E)
Expression of inhibin-
was not affected in mutant ovaries. (F) The
expression pattern of Amh, which is implicated in the activation of
primordial follicles, exhibits significantly reduced expression levels in
Foxl2lacZ homozygous mutant ovaries. (G)
Gdf9 expression starts at the type 3a follicle stage in WT oocytes.
In the 2-week-old Foxl2lacZ homozygous mutant
ovary all oocytes express Gdf9, including regions that correspond
histologically to Fig. 5B. (H)
Kitl is expressed in pregranulosa and granulosa cells during
folliculogenesis. In Foxl2lacZ homozygous mutant
ovaries Kit ligand expression is maintained at all stages. At least
three different ovaries were analysed per time point.