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Fig. 7. Loss of PS1, but not PS2, integrin function phenocopies perd
loss-of-function in muscles. Each row shows the development of a single
embryo injected with dsRNA from the time GFP expression in muscle VL1 first
becomes detectable (t=0, approximately stage 14) through late stages,
when muscles are contracting and embryos are moving. Additional GFP expression
comes from visceral muscles that also express Gal4, internally to the VL1
muscle. Scale bar: 50 µm. (A-D) In control lacZ
dsRNA-injected embryos, muscles are initially unattached, but rapidly achieve
their mature attachment sites (B) and elongated morphology (C). (E-H)
RNAi directed against perd prevents muscles from ever forming proper
attachments. (I-L) Grip dsRNA affects fewer muscles, with a
timecourse similar to that of perd. (M-P) RNAi for the
PS1 integrin subunit mew, which affects both maternal and
zygotic transcripts, causes a severe phenotype identical to that of
perd. By contrast, in embryos injected with dsRNA for the PS2
subunit if (Q-T), many muscles develop apparently normal
attachments and elongated morphology at stage 16 (arrowheads in S) before
assuming a rounded-up appearance after muscle contraction begins (arrowheads
in T). Removal of both PS integrins by RNAi directed against the common β
subunit mys (U-X) gives the more severe early phenotype.
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