The In Vivo Function of Müllerian-Inhibiting Substance During Mammalian Sexual Development

2001 ◽  
pp. 41-59
Author(s):  
Yuji Mishina
Cell ◽  
1994 ◽  
Vol 79 (3) ◽  
pp. 415-425 ◽  
Author(s):  
Richard R. Behringer ◽  
Milton J. Finegold ◽  
Richard L. Cate

2002 ◽  
Vol 99 (1) ◽  
pp. 239-244 ◽  
Author(s):  
D. L. Segev ◽  
Y. Hoshiya ◽  
M. Hoshiya ◽  
T. T. Tran ◽  
J. L. Carey ◽  
...  

1998 ◽  
Vol 158 (1) ◽  
pp. 1-6 ◽  
Author(s):  
AH Lane ◽  
PK Donahoe

The primary function of MIS in mammals is to initiate regression of Mullerian structures in males as part of normal sexual development. As we learn more about its other roles, particularly its influence on the growth and differentiation of cell types within the gonad, a more thorough understanding of the receptors that MIS stimulates and the downstream signaling cascade with which it interacts will help in the development of diagnostic and therapeutic uses of MIS.


2006 ◽  
Vol 12 (5) ◽  
pp. 1593-1598 ◽  
Author(s):  
Rafael Pieretti-Vanmarcke ◽  
Patricia K. Donahoe ◽  
Paul Szotek ◽  
Thomas Manganaro ◽  
Mary K. Lorenzen ◽  
...  

Nature ◽  
1990 ◽  
Vol 345 (6271) ◽  
pp. 167-170 ◽  
Author(s):  
Richard R. Behringer ◽  
Richard L. Cate ◽  
Glenda J. Froelick ◽  
Richard D. Palmiter ◽  
Ralph L. Brinster

Development ◽  
1997 ◽  
Vol 124 (9) ◽  
pp. 1799-1807
Author(s):  
G. Giuili ◽  
W.H. Shen ◽  
H.A. Ingraham

Mullerian Inhibiting Substance (MIS) functions to promote regression of the Mullerian duct during male development. Maintaining the sexually dimorphic pattern of MIS expression is essential for proper mammalian reproductive tract development. Here, we show that the intricate spatial and temporal pattern of MIS expression is directed by a remarkably small proximal promoter of only 180 base pairs in length. Expression of the MIS-human growth hormone transgene (MIS/GH) is restricted to Sertoli cells in embryonic testis and to granulosa cells of postnatal ovary, consistent with the known MIS expression pattern. The proximal MIS promoter is therefore sufficient to direct the initiation and the maintenance of MIS gene expression in both sexes. Moreover, in vivo MIS promoter activity requires an intact binding site for the orphan nuclear receptor SF-1. Taken together, these data strongly suggest that SF-1 directly activates MIS in embryonic and postnatal gonads. Consistent with the proposed role of SF-1 in mammalian sex-determination, our study provides physiological evidence that a SF-1 binding site is essential for gene activation of an embryonic testis-specific marker.


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