Figure 6

The EGFR pathway is required in enterocytes for proper gut morphogenesis. (a) Midguts with enterocytes depleted of the EGFR pathway (Myo1AGal4, UAS-EGFR^DN) are longer and thinner than WT guts. Conversely, guts from flies expressing a constitutive form of EGFR are shorter and wider. The effect of EGFR is most pronounced in the copper cell region (borders of which are indicated with asterisks). Representative images were taken of dissected guts from 3-day-old to 4-day-old flies stained with DAPI. Guts from flies expressing a constitutive form of EGFR are approximately half the length of WT UC flies. (b) Nuclear staining of guts with EGFR-deficient enterocytes reveals a decrease in cell density and flattening of nuclei as compared to WT guts. Quantification of the mean distance between the nearest adjacent nuclei in WT and EGFR-depleted guts. Measures were taken in the region around the copper cells (middle midgut), where the effect of EGFR is most pronounced (Additional file 11C). Additionally, the orientation of the distance vector between the two nearest nuclei switches from longitudinal to transversal, indicating a change in epithelial geometry (see model, Additional file 11D). (c) Relative length of WT guts, guts with enterocytes depleted for the EGFR pathway or guts with activated EGFR in enterocytes. Constructs were placed under the control of a thermosensitive enterocyte driver (Myo1AGal4^TS). Adult flies were switched from 18°C (Gal4 nonfunctional) to 29°C (Gal4 functional) 3 days before infection or before initial measurements were taken. Guts depleted for the EGFR pathway (UAS-EGFR^DN or UAS-Ras^DN) in enterocytes shrink less upon infection with Ecc15. After a recovery phase of 2 or 8 days, the guts are 25% longer than their WT counterparts. Conversely, guts of flies with ectopic activation of EGFR (UAS-EGFR^ACT) in enterocytes do not elongate in response to infection and are 40% shorter than WT guts.