Figure 1
Figure 1. nop10 loss results in ribosome biogenesis defects affecting the small ribosomal subunit. (A) Semiquantitative PCR analysis on wild-type versus nop10 mutants at 4 dpf using nop10 or actin primers. (B) Gross morphology of the nop10 mutant compared with a wild-type sibling from 1 to 4 dpf. Arrow indicates dent in mid-hind brain barrier; and arrowhead, pericardial edema. (C) A contemporary schematic illustrating the major pathway of rRNA processing in zebrafish. Hybridization sites of ITS-1, ITS-2, and 18S probes are indicated on top. Arrowheads indicate major cleavage sites. (D) Northern blot analysis of total RNA isolated from nop10 mutants compared with wild-type siblings at 4 dpf using probes against ITS-1, ITS-2, and 18S. (E-F) Polysome profiles of wild-type siblings (E) compared with nop10 mutants (F) at 4 dpf. The 40S, 60S, 80S, and polysomal peaks are indicated.

nop10 loss results in ribosome biogenesis defects affecting the small ribosomal subunit. (A) Semiquantitative PCR analysis on wild-type versus nop10 mutants at 4 dpf using nop10 or actin primers. (B) Gross morphology of the nop10 mutant compared with a wild-type sibling from 1 to 4 dpf. Arrow indicates dent in mid-hind brain barrier; and arrowhead, pericardial edema. (C) A contemporary schematic illustrating the major pathway of rRNA processing in zebrafish. Hybridization sites of ITS-1, ITS-2, and 18S probes are indicated on top. Arrowheads indicate major cleavage sites. (D) Northern blot analysis of total RNA isolated from nop10 mutants compared with wild-type siblings at 4 dpf using probes against ITS-1, ITS-2, and 18S. (E-F) Polysome profiles of wild-type siblings (E) compared with nop10 mutants (F) at 4 dpf. The 40S, 60S, 80S, and polysomal peaks are indicated.

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