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Fig. 8. Xtes MO depletion causes defects in somitogenesis and AP patterning. Axis elongation was examined by immunostaining for either (A–D) notochord using the
monoclonal antibody MZ15, which recognizes keratan sulfate, or (E–H) with 12–101, which recognizes differentiated muscle. Embryos were either (A, E) uninjected
or injected at the 1 cell stage with 80 ng of (B, F) Xtes ConMO1, (C–G) Xtes MO1 or (D–H) Xtes MO2. (I–K) 12–101 immunostaining of embryos injected with
40 ng of either (I) Xtes ConMO1 or (J, K) Xtes MO1. The 12 somites formed during gastrulation are indicated with a white arrowhead in panels I and J, with the 20th
somite also indicated in panel I. Xtes MO1-injected embryos displayed either (J) a weak patterning defect in the first 12 somites or (K) a complete loss of somitic
patterning, but in both cases (J, K) postgastrulation somitogenesis was disrupted. (L–W) The expression patterns of various genes expressed during tail bud stages (L,
P, T) FGF8, (M, Q, U) Xdelta-1, (N, O, R, S, V, W) and Xcad3 were determined by in situ hybridization at (L–N, P–R, T–V) stage 20 in embryos injected at the 1 cell
stage with either (L–N) Xtes ConMO1, (P–R) Xtes MO1 or (T–V) Xtes MO2. Note the loss of rostral FGF8 staining (white bracket) in (P) Xtes MO1 and (T) Xtes
MO2-injected embryos compared to (L) embryos injected with Xtes conMO1. White arrows in panels M, Q and U denote somitic expression of Xdelta-1. Expression
of Xcad3 in stage 28 embryos injected with either (O) Xtes conMO1, (S) Xtes MO1 or (W) Xtes MO2. The white arrowhead in panel O denotes the most rostral
expression of Xcad3 in the neural tube. |
