Figure 1.

Infection upregulates immune genes in periostial haemocytes. (a) The heart with periostial haemocytes, the circulating haemocytes and the abdomen of mosquitoes that were naive, injured or infected with GFP-E. coli or S. aureus were sequenced by RNAseq at 4 h post-treatment. (b) Fluorescence and DIC overlay shows that the periostial haemocytes (CM-DiI; red) remain attached to a resected heart (phalloidin; green). Marked are the periostial regions for each abdominal segment, the thoraco-abdominal (T-A) ostia and the posterior excurrent opening. Image is modified from Sigle & Hillyer [7], and reproduced according to Creative Commons Attribution License CC BY. (c) Naive and injured mosquitoes have resident periostial haemocytes, but infection for 4 h with GFP-E. coli or S. aureus induces the aggregation of additional haemocytes at the periostial regions. Whiskers show the standard error of the mean (s.e.m.; n = 14 for all groups). (d) Bar plots show the number of genes significantly upregulated or downregulated at 4 h after GFP-E. coli or S. aureus infection in the periostial haemocytes and heart (left), the circulating haemocytes (middle) and the entire abdomen (right). (e) Venn diagrams show that 55, 21 and 15 genes are significantly upregulated in the periostial haemocytes, the circulating haemocytes or the abdomen, respectively, during both GFP-E. coli and S. aureus infections. (f) Table listing the immune genes that are among the 55 genes that were upregulated in the heart with periostial haemocytes following both GFP-E. coli or S. aureus infection. Genes that participate in the IMD and JNK pathway are in bold.