These results suggest that the sg2 mutant phenotype is due to two recessive mutations, simultaneously.
The segregation ratio (3:1) of green to albino plants showed that the mutant phenotype is controlled by a single recessive gene (tcm5) (Additional file 2: Table S2).
The mnt mutant phenotype is caused by a complete loss of function of the AUXIN RESPONSE FACTOR 2 (ARF2), which encodes a transcription factor mediating gene expression in response to auxin.
The oto mutant phenotype is consistent with our biochemical studies.
The mutant phenotype is caused by a single base deletion in the gene inositol polyphosphate 4-phosphatase type I (Inpp4a) [1].
An additional question that arises from the inspection of the T192 mutant phenotype is the specific origin of the dramatic reduction of the P110 levels.
The sk8 mutant phenotype is first visible around 19 hpf, suggesting the presence of maternal Foggy protein at earlier stages of development.
Our discovery that the Lrig3 mutant phenotype is apparently unrelated to NRG signaling emphasizes the need to confirm the relevance of each of these in vitro binding interactions for specific in vivo functions.
Together, these studies indicate that the hsp90α1 mutant phenotype is not simply due to disruption of myosin folding and assembly, suggesting that Hsp90α1 may play a role in the assembly and organization of other sarcomeric structures.
As expected, we found that loss of kelch caused a range of defects in dendritic branching (Figure 4), confirming that kelch mutant phenotype is not fully penetrant in neurons.
Together, these studies demonstrated loss of myosin function resulted in a different effect than hsp90α1 mutation on myofibril organization, suggesting the hsp90α1 mutant phenotype is not simply due to disruption of myosin folding and assembly.
