Fig. 1

Loss of Kdm2aa function leads to growth and oogenesis defects.

(A) The zebrafish paralogues Kdm2aa and Kdm2ab share the protein domain structure with their human orthologue KDM2A. The mutations kdm2aa^sa898 and kdm2aa^sa9360 produce premature stop codons in the JmjC and F-box domain, respectively. The allele kdm2ab^sa1479 produces a premature stop codon in the JmjC domain. (B) Juvenile fish compound heterozygous for kdm2aa^sa898 and kdm2aa^sa9360 are shorter and thinner at 30 d.p.f. than their heterozygous siblings. Scale bar: 5 mm. (C) Box plots showing length in mm of each of the three sibling groups for a representative family at 30, 90 and 180 d.p.f. Fish homozygous for kdm2aa^sa898 are smaller than their siblings. (D) Fish homozygous for premature stop codons in kdm2aa represent less than the expected 25% of the group. (E) A small proportion of maternal zygotic kdm2aa^sa9360 embryos survive to 5 d.p.f. with mild (arrow in second panel) or no malformations (bottom panel). (F) Embryos derived from kdm2aa^{sa9360/sa9360} intercrosses show severe defects and lethality during the first 24 h.p.f. whereas kdm2aa^{sa9360/sa9360} male outcrosses are normal. (G) Two examples of embryos derived from kdm2aa^{sa9360/sa9360} female outcrosses displaying severe defects at 24 h.p.f. (H) TRITC-Phalloidin and DAPI staining on MZkdm2aa^-/- embryos derived from intercrosses of kdm2aa^sa898/sa9360 fish at the 8–16 cell stage showed that despite cell asymmetry and asynchronous division, nuclei seemed overall normal. (I) Expression data from Expression Atlas http://www.ebi.ac.uk/gxa/experiments/E-ERAD-475 showing normalised counts (FPKMs) from RNA-seq data for kdm2aa and kdm2ab. There is maternal contribution of both genes, but kdm2ab polyA transcript abundance peaks at early blastula stages, whereas kdm2aa polyA transcript abundance peaks later at the gastrula shield stage.