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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Jumu is required for circulating hemocyte differentiation and phagocytosis in Drosophila

Fig. 3

Loss of jumu or NimC1 in circulating hemocytes causes filopodia defects. a-d Phalloidin staining (green) of circulating hemocytes shows a reduced number and length of filopodia in jumu mutant hemocytes compared with those in the controls. The arrow shown in D indicates an enlarged round hemocyte, and the asterisk shown in d indicates a lamellocyte. e-h Phalloidin staining (green) of circulating hemocytes isolated from third-instar larvae injected with latex beads (red). The jumu mutants show filopodium defects (f-h), although a portion of the enlarged round hemocytes (arrow) and lamellocytes (asterisk) exhibit an elongation of filopodia in the jumu double heterozygotes (h). i, j Quantification of the number (i) and length (j) of filopodia. k-p Phalloidin staining (green) of circulating hemocytes shows a reduced number and length of filopodia in jumu or NimC1 knockdown hemocytes compared with those in the control (l, n), and the overexpression of jumu or NimC1 can rescue the number and length of filopodia in the jumu knockdown hemocytes (m, p). q, r Quantifications of the number (q) and length (r) of filopodia. Error bars represent the S.E.M; * P < 0.05; **P < 0.01; ***P < 0.001 (one-way ANOVA). Scale bars: 10 μm

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