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Fig. 10. lmx1b.1 and lmx1b.2 cooperate with other IsO genes to
maintain cell survival in the caudal MMR. (A) During IsO maintenance in
wild-type embryos, Lmx1b.1 and Lmx1b.2 maintain wnt1, wnt3a and
wnt10b expression at the caudal edge of the mesencephalic vesicle.
fgf8 is expressed in an adjacent domain in the rostral metencephalic
vesicle. pax2.1, pax5 and pax8 are expressed in a broader
domain that encompasses the caudal mesencephalon and rostral metencephalon.
When Lmx1b.1/2 activity is knocked down with morpholinos, increased apoptosis
is observed, not in the lmx1b.1/2 expression domain, but in the
adjacent region of the MMR, including the normal fgf8 domain. By
contrast, loss of Pax2.1 function in noi mutant embryos results in
increased apoptosis concentrated in the rostral region of the MMR. These data
indicate that the IsO produces signals that maintain cell survival in an
asymmetric, non-cell-autonomous manner. (B) The data presented are consistent
with a model in which Lmx1b.1 and Lmx1b.2 maintain cell survival at the MMR by
regulating fgf8, wnt1, wnt10b and wnt3a, secreted factors
whose loss precipitates apoptosis in the MMR
(Buckles et al., 2004;
Jászai et al., 2003).
Lmx1b.1/2 may maintain fgf8 by regulating expression of wnt1,
wnt3a, wnt10b, pax8 or an alternative mechanism. Fgf8, in turn, functions
in a positive feedback loop to maintain lmx1b.1/2 expression.
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