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First published online 30 November 2006
doi: 10.1242/dev.02697
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1 Department of Genetics, National Institute of Genetics, SOKENDAI, 1111 Yata,
Mishima, Shizuoka 411-8540, Japan.
2 Division of Mammalian Development, National Institute of Genetics, SOKENDAI,
1111 Yata, Mishima, Shizuoka 411-8540, Japan.
3 Core Research for Evolutional Science and Technology (CREST), Japan Science
and Technology Corporation, 2-6-15, Shibakoen, Minato-ku, Tokyo 105-0011,
Japan.
Author for correspondence (e-mail:
ysaga{at}lab.nig.ac.jp)
Accepted 16 October 2006
The mouse Nanos proteins, Nanos2 and Nanos3, are required for germ cell
development and share a highly conserved zinc-finger domain. The expression
patterns of these factors during development, however, differ from each other.
Nanos3 expression in the mouse embryo commences in the primordial germ cells
(PGCs) just after their formation, and a loss of this protein results in the
germ cell-less phenotype in both sexes. By contrast, Nanos2 expression begins
only in male PGCs after their entry into the genital ridge and a loss of this
protein results in a male germ cell deficiency, irrespective of the
co-expression of Nanos3 in these cells. These results indicate that these two
Nanos proteins have distinct functions, which depend on the time and place of
their expression. To further elucidate this, we have generated transgenic
mouse lines that express Nanos2 under the control of the Oct4
PE
promoter and examined Nanos2 function in a Nanos3-null genetic
background. We find that ectopically produced Nanos2 protein rescues the
Nanos3-null defects, because the germ cells fully develop in both
sexes in the transgenic mice. This result indicates that Nanos2 can substitute
for Nanos3 during early PGC development. By contrast, our current data show
that Nanos3 does not rescue the defects in Nanos2-null mice. Our
present findings thus indicate that there are redundant functions of the Nanos
proteins in early PGC development, but that Nanos2 has a distinct function
during male germ cell development in the mouse.
Key words: Primordial germ cell, Transgenic mouse, Oct4 enhancer, Antibody, Genetic rescue, Spermatogenesis