Figure 1. Age-associated inflammation in fat body may repress IMD signaling in the midgut.
A. Adult Drosophila dorsal abdomen. Adult fat body cells (red) align the inner cuticle surface of abdominal segments (A1-6). The oenocytes (blue), cardiac tube with its peripheral cells (green), foregut, midgut, and hindgut are also shown. Gut with the indicated midgut segments (posterior P1-3 and P4) and Malpighian tubules (MT) attached to the posterior end of P4 are to the right. All immunofluorescence images of fat body and midgut in this manuscript are from A4 (black dashed box) and P4 (red box), respectively.
B. Selected up- or down-regulated genes involved in the IMD pathway upon aging in fat body or midgut, respectively. Numbers and color-codes indicate fold changes. A simplified IMD signaling pathway is shown to the right.
C–D. qRT-PCR analyses of PGRPs, LB, SC1, and SC2, in fat body (C) and midgut (D) from young and old wild-type (WT) flies. Expression in old organs was plotted relative to the young. Error bars, Standard error of the mean (SEM) from three independent experiments. Student’s t-tests, *p<0.05, **p<0.01, ***p<0.001.
E–H. Dpt-lacZ reporter assay of fat bodies (E, F) or midguts (G, H) from young (E, G) or old flies (F, H). Dpt-lacZ was only in peripheral cells in all (15) young fat bodies (white arrow in E), but was throughout 11 of 17 old fat bodies (F). 12 of 15 old midguts (H) had reduced Dpt-lacZ compared to that of the young (G, 12 analyzed).
I–J. REL (green or white) is mostly cytoplasmic in young (I) or nuclear (DAPI, red) in old (J) fat body cells.
K–N. Young control midguts (K) had nuclear REL, which was reduced by 50 days (L). Depletion of REL (M) or co-depletion of PGRP-SC2 plus PGRP-LB (N) by RNAi in fat bodies restored nuclear REL staining in old midguts.
Scale bars, 20 μm.