Golgi complex ultrastructure is disrupted in the ffr digestive tract.
2
These data indicate that ffr is required for both Golgi structure and vesicular trafficking, and ultimately lipid transport.
3
The zebrafish fat-free (ffr) mutation was identified in a physiological screen for genes that regulate lipid metabolism.
4
Through positional cloning, we have identified a causative mutation in a highly conserved and ubiquitously expressed gene within the ffr locus.
5
Enterocyte retention of an endosomal lipid marker in ffr larvae support the idea that altered vesicle trafficking contributes to the ffr mutant defect.