High impact information on hoxb1a

• Second, vhnf1 functions independently of Fgf signals to repress hoxb1a expression [1].
• We have used a morpholino-based knockdown approach to investigate the functions of a pair of zebrafish Hox gene duplicates, hoxb1a and hoxb1b, which are expressed during development of the hindbrain [2].
• However, using an RNA rescue approach, we reveal that these duplicated genes do not have interchangeable biochemical functions: only hoxb1a can properly pattern the VIIth cranial nerve [2].
• Knockdown of duplicated zebrafish hoxb1 genes reveals distinct roles in hindbrain patterning and a novel mechanism of duplicate gene retention [2].
• Despite this difference in protein function, we provide evidence that the hoxb1 duplicate genes were initially maintained in the genome because of complementary degenerative mutations in defined cis-regulatory elements [2].

Biological context of hoxb1a

• Moreover, the hoxb1 duplicate genes have differing functional capacities, suggesting divergence after duplication [3].

Anatomical context of hoxb1a

• We find that Hoxb1b and Pbx4 act together to induce ectopic hoxb1a expression in rhombomere 2 of the hindbrain [4].
• Consistent with this, lzr/pbx4 interacts genetically with hoxb1a to control facial motor neuron migration [5].

Other interactions of hoxb1a

• Using genetic mosaic analysis, we show that lzr/pbx4 and hoxb1a are primarily required cell-autonomously within the facial motor neurons; however, analysis of a subtle non-cell-autonomous effect indicates that facial motor neuron migration is promoted by interactions amongst the migrating neurons [5].

References