Impairing follicle-stimulating hormone (FSH) signalingin vivo: Targeted disruption of the FSH receptor leads to aberrant gametogenesis and hormonal imbalance

Abstract

authors request that the following corrections be noted. It was accidentally stated that the studies by Kajita et al. (1) and Lee et al. (2) dealt with cinnamoyl-CoA reductase modified plants when in fact they concerned 4-coumarate:coenzyme A ligase (4CL) transgenic plants. Lignin concentration was reduced by down-regulation of 4CL activity in both studies (1, 2). In a subsequent article, Kajita et al. (3) reported a negligible decrease in lignin concentration and a decreased syringyl-toguaiacyl ratio for lignin composition of a sense-suppressed 4CL transgenic tobacco line. Kajita et al. (1) rather than Kajita et al. (3) was inadvertently cited when this later report was contrasted with the large decreases in lignin concentration and an increased syringyl-to-guaiacyl lignin ratio for anti-sense suppressed 4CL Arabidopsis transgenics (2). The authors apologize for the confusion these errors have created for readers of their Commentary and to the authors of the cited work for misrepresenting their research. November 10, 1998, of Proc. Natl. Acad. Sci. USA (95, 13612-13617), the authors request that the following correction be noted: In Fig. 2 appearing on page 13614, the genotype identification for testicular histology in panels C and D were shown reversed. The correct identification is Ϫ͞Ϫ for panel C and ϩ͞ϩ for panel D. The fifth sentence of the figure legend should read as follows: "Histological sections at lower (E) and higher (D) magnification of the seminiferous tubuli from a wild-type and mutant (F and C) mouse."Cell Biology. In the article "Efficient construction of a large nonimmune phage antibody library: The production of highaffinity human single-chain antibodies to protein antigens" by

Regulation of testicular function in men: implications for male hormonal contraceptive development

“…The contrast with LH-␤ mutations [12] implies that either the LH receptor itself or constitutively produced T has a role in male fetal sexual differentiation. Inactivating mutations in the FSH receptor result only in oligozoospermia with reduced testicular size and normal fertility [16], similar to the phenotypes observed in FSH-␤ and FSH-receptor knockout mice [17,18]. This finding implies that the presence of FSH is not an absolute requirement for the pubertal initiation and maintenance of spermatogenesis or fertility, a conclusion identical to that ascertained in the FSH and LH depletion experiments in man described above.…”

Mechanisms involved in the homologous down-regulation of transcription of the follicle-stimulating hormone receptor gene in Sertoli cells

“…One of the most important biochemical signaling networks involved in controlling normal spermatogenesis in mammals exists between the anterior lobe of the pituitary gland and Sertoli cells in the testis (Griswold et al, 1975(Griswold et al, , 1976(Griswold et al, , 1977Orth, 1984;Singh and Handelsman, 1996;Kumar et al, 1997;Tapanainen et al, 1997;Dierich et al, 1998). The biological events controlled by this endocrine mechanism result from the interaction of follicle-stimulating hormone (FSH) with the FSH receptor and the subsequent transduction of molecular information across the membrane leading to the production of second messengers such as cAMP (Means et al, 1980) and Ca 2 + (Chaudhary et al, 1996;Lalevee et al, 1999) and changes in gene expression.…”

Follicle stimulating hormone‐induced growth promotion and gene expression profiles on ovarian surface epithelial cells

“…1 Follicle stimulating hormone (FSH), through interaction with its specific receptor, FSHR, plays an essential role in mammalian reproduction and ovarian folliculogenesis. 2 Binding of FSH to FSHR results in adenylyl cyclase activation leading to cAMP synthesis, associated with intracellular rise of Ca 2ϩ , activation of protein kinase A (PKA) and other downstream signal transduction pathways. [2][3][4][5][6] It has been reported that FSH treatment stimulates cell proliferation on normal human OSE cells, immortalized OSE cells and OC cell lines.…”

“…2 Binding of FSH to FSHR results in adenylyl cyclase activation leading to cAMP synthesis, associated with intracellular rise of Ca 2ϩ , activation of protein kinase A (PKA) and other downstream signal transduction pathways. [2][3][4][5][6] It has been reported that FSH treatment stimulates cell proliferation on normal human OSE cells, immortalized OSE cells and OC cell lines. 7,8 However, little has been known on the effects of FSH in the process of tumorigenesis and growth stimulation on human OSE at molecular levels.…”