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Fig. 5. fozi-1 acts downstream of the bi-stable feedback loop to
control ASER differentiation. (A) Asymmetric fozi-1::gfp
expression (otEx2192; line #3 in
Fig. 3C) is disrupted in
die-1(ot26), lsy-6(ot71) and cog-1(sy607) null mutants
animals, and partially affected in lim-6-null mutants. The `L=R'
category indicates equal expression in ASEL and ASER, including de-repression
of gfp expression in ASEL (yielding strong gfp expression in
both ASEL and ASER; die-1 and lsy-6 phenotype) and reduction
of gfp expression in ASER (yielding equally low expression in ASEL
and ASER; cog-1 phenotype). (B) Removing fozi-1
reverts the loss of lim-6 expression (otIs114) observed in
lsy-6(ot71) or die-1(ot26) mutant animals. (C)
Summary of genetic interactions, pooling data from A and B, combined with the
data from Fig. 4. The
completely penetrant and expressive phenotype observed in die-1
mutants argues that the pathways parallel to fozi-1 and
lim-6 are under die-1 control. The simplest explanation is
that die-1 itself acts in parallel to fozi-1 and
lim-6 to control expression of target genes. (D)
fozi-1(cc607) null mutant animals display weakly penetrant defects in
lsy-6 expression, assayed with lsy-6prom::gfp
(otIs162) and cog-1 expression, assayed with cog-1::gfp
(syIs63). (E) Summary of the feedback data. The lim-6-
dependent feedback to lsy-6 (or die-1; for simplicity, the
arrow only points to lsy-6), described in Johnston et al.
(Johnston et al., 2005), is
represented by a broken arrow to indicate that the effect is partially
penetrant and only required to maintain the asymmetric expression of loop
components.
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