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We observed no Nodal expression in the LPM mesoderm of mutant embryos, however, the downstream target, Pitx2, was expressed in the LPM in a minority of mutant embryos.

We investigated its role in morphogenesis by looking at aPKC mutant embryos, however we did not observe a strong phenotype in denticle formation or alignment.

We observed a robust neuronal expression of TRE-eGFP in puc mutant embryos; however, not all of these neurons died as suggested by the quantification of DAC-positive neurons.

We observed regional swellings of the extracellular matrix in the AVC and OFT (Fig. 9C-F) of the heart in both control and mutant embryos; however, invasion of the mesenchyme was dramatically decreased in the mutants (Fig. 9D,F).

In ttk mutant embryos, however, the enhancer shows a dramatic derepression (Fig. 5J,J′,L,L′), in both the somatic and visceral mesoderm, as well as in the ectoderm and endoderm (compare Fig. 5I,I′ with 5J,J′ and 5K,K′ with 5L,L′).

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EED-mutant embryos, however, show increased and frequent reactivation of an Xp-linked green fluorescent protein (GFP) transgene in cells of both the VE and the PE [ 24].

However, when wild type embryos undergo M16 at 6.5 7 hr AEL, His C mutant embryos still failed to express string but 2xHis-GU embryos upregulated string expression.

In these mutant embryos, hair cell differentiated; however, their distribution pattern was slightly disorganized in the cochlea where the growth of type II nerve fibers to outer hair cells along Prox1 expressing supporting cells was severely disrupted.

Sequencing of 18S rRNA in wild-type and kri1l cas002 mutant embryos showed no difference; however, 80S ribosome and polysome formation were impaired in kri1lcas002 mutant embryos with excessive 60S ribosome subunits (Supplementary information, Figure S9D).

However, homozygous mutant embryos could not be repaired in way because of the lack of WT alleles.

However, the mutant embryos analyzed showed an average index of only 43.1% (with a SEM of 6.7%) (Figure 4A4 and 4B), suggesting a significantly impaired cell proliferation capacity in mutant embryos in vivo.

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