This phenotype is similar to those reported by Gallagher et al. upon RBFOX1/2 knockdemonstratingsthatinhibitionnhibitiof of the RNA binding properties of RBFOX1/2 proteins by the decoy oligonucleotides and the concomitant change in alternative splicing, result in a delayed muscle development phenotype in vivo.
Our results present multiple lines of evidence suggesting links between modules and muscle phenotypes, and provide insights into the molecular bases of genome organization in muscle development and phenotype variation.
These data led us to examine a potential role of the direct mitochondrial pathway in in vivo muscle development and phenotype.
These findings are important in elucidating the molecular mechanisms that underlie muscle development and phenotype variation, and reveal the potential impact of evolutionary changes at the coexpression network level.
The most significant phenotypes observed were related to the nervous system and muscle development, but no enrichment for phenotypes related to sexual differentiation was observed (data not shown).
This comparison showed a close resemblance between the Nes-Cre Wt1co mutants and the WT1-mutant tumours, especially with respect to the ectopic muscle development signature, whereas the phenotype in the Pax8+/Cre Wt1co mutant kidneys more resembled the one found in WT1-wild-type Wilms' tumours.
Compensatory mechanisms and redundancy with GLP might account for the lack of an overt phenotype in muscle development in vivo upon conditional ablation of G9a in the skeletal muscle45.
These negative coexpression network modules associated with muscle development might control the muscle phenotype in LT, which features low lean meat percentage, slow-growing muscle and low body weight.
Analysis of pat-9 showed it is expressed early in development and within body wall muscle lineages, consistent with a role in muscle development and producing a Pat phenotype.
