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The enhancement of silencing seen in the dcl4 mutants might indicate some inhibitory role of DCL4 or an earlier onset of silencing due to the accelerated juvenile-to-adult transition seen in these mutants [22], [23].
Hence the shorter period observed in the double mutants might indicate that the concomitant absence of these two clock genes has a cumulative effect on circadian period in DD.
The aberrant coexpression of intermediate markers, K8 and K19, in the Bmpr1a-CKO mutants might indicate that Bmp signaling is required for epithelial differentiation of intermediate cells to luminal cells.
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Not least important, the strong increase in the number of molecules in the nodD4 mutant might indicate that the gene is a repressor of other regulatory genes, such as nodD1 (Additional file 1: Table S1, Additional file 2: Table S2 and Additional file 3: Table S3).
Our findings demonstrate significant differences in the immune response profiling of Wt α-Syn and PD-related mutants that might indicate the existence of different pathways towards PD onset and progression.
As this site was reported to be possibly involved in higher-order Wnt-CRD complexes, the increase in Wnt activity in Wnt3a mutant proteins might indicate that oligomerization leads to a depletion of active Wnt ligands.
Considering the role of MeCP2 as a transcriptional regulator, we wondered whether the alteration in GRID1 expression in the MECP2-mutant clone might indicate that MeCP2 protein directly binds to the GRID1 promoter to regulate its expression.
The increased growth of the ssaN mutant in HLA-B27 cells might indicate that this mutant has good fitness in HLA-B27-positive U937 cells.
Increased growth of the ssaN mutant in HLA-B27-positive cells might indicate a special connection between this mutant and HLA-B27-positive cells, and may even be relevant to the pathogenesis of HLA-B27-associated ReA.
These factors might indicate that the mutant strain carries a more positive charge than the WT [ 17, 28].
Thus, the absence of anaemia in most FA mouse models might indicate that FA mutant mice housed in laboratory conditions are protected from stressful environmental cues that might contribute to BMF in humans with FA.
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