In mutant animals we observed a slight decrease in mechanical withdrawal threshold, even if two-way ANOVA for repeated measures showed a significant main effect for time (F 7,133) = 4,735; P < 0.01 and F 7,147) = 2,491; P < 0.01 for females and males, resp).
In addition, a disorganization of the sarcomeric muscle architecture in ΔC3GMS mutant animals can be observed using the Z-band specific reporter Zasp-GFP [23] (Figure 4G and H; arrow).
However, alteration of the expression of different neuropeptides in mutant animals has been observed, such as upregulation of neuropeptide Y (NPY) by ∼30-fold in the dorsomedial-ventromedial hypothalamus (DMH/VMH) of mature tubby mice [9], as well as altered expression of the agouti-related protein (AGRP) in the ARC nuclei of the hypothalamus [8].
There was no reduction in the mass of ATPalpha CJ mutant animals as is observed in eat-6 mutants (Supplemental Fig. 4).
Along with tissue deterioration per se, this was the only phenotype that was specific to the mutant animals, and never observed in normal aging.
These differences between control and mutant animals were already observed in neonates, but became more apparent during postnatal development (Fig 1A C; Supplementary Fig S2A and B).
Thus we found that expression of TBPHF/L150 152 using D42-GAL4 in TBPHD23 homozygous flies failed to recover the anatomical defects observed in mutant animals regarding the number of synaptic boutons, synaptic branches and MTs organization (Figure 6C G).
Dock1- and Rac1-null mammary glands failed to activate properly Stat3 such that a delay in the morphologic changes associated with involution was observed in mutant animals.
The effect of the LAB consortium on fat deposition (data not shown) and on the lifespan of the mutant animals was similar to that observed with the N2 strain).
Furthermore, restoration of Crim1 levels in just the lens tissue of Crim1KST264 mice is sufficient to ameliorate most of the dysgenesis observed in the mutant animals.
