To confirm that YFP distribution represented completely the morphology of astrocytes, we used the method that was described previously [31, 32], and injected Alexa Fluor 568, which has smaller molecular weight into YFP-labeled cells in fixed brain slices. As shown in Supplementary Figure S5a and b, both Alexa Fluor 568 and YFP labeled astrocytic cell bodies and fine processes. However, because of labeling the cell at living status, YFP distribution exhibited more complete morphology than the injected fluorescent dye did (Supplementary Figure S5a and b). Therefore, YFP labeling would reliably help us to evaluate the astrocytic sizes in mouse cortices. Four days after injury, more reactive astrocytes in the injured cortices of both Mlc1-dnEGFR and littermate mice expressed detectable GFAP, as all cells targeted by AAV-TRE-YFP were immunopositive for GFAP (Figure 2h). Suppression of hypertrophy in reactive astrocytes in Mlc1-dnEGFR cortices was more striking when cell sizes were measured according to the distribution of YFP fluorescence, in comparison with that based on GFAP immunoreactivity (Figure 2h). Four and 8 days after injury, the YFP-labeled reactive astrocytes in Mlc1-dnEGFR cortices exhibited sizes 28.06±10.3% and 47.30±14.6%, respectively, of those in littermate controls (Figure 2i). Taken together, these results suggested that the morphological reaction of astrocytes was more likely to depend on actin remodeling than intermediate filament extension. Further, these findings revealed that the regulation of this hypertrophic remodeling was ErbB dependent.