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. 2021 Aug 9;22(9):e52262. doi: 10.15252/embr.202052262

Figure 3. The NimB4sk2 mutant is defective in cell corpse clearance.

Figure 3

  1. Representative confocal imaging of wild‐type (w1118), NimB4sk2 , and apoptosis‐null NimB4sk2; Df(3L) H99 embryonic macrophages at stage 16 of development; ventral and lateral view; Tissues were co‐stained with Dcp‐1 (red, corresponding to apoptotic corpses) and anti‐SIMU (green, corresponding to macrophages) antibodies. The arrows show the presence of apoptotic cells inside embryonic macrophages. Scale bars = 20 μm.
  2. Quantification of caspase‐positive particles (anti‐Dcp‐1, red) within macrophages (anti‐SIMU, green). Values from at least five independent experiments are represented as mean ± SD total volume of caspase‐positive particles (**P < 0.01, by Mann–Whitney test).
  3. Representative projections from confocal stacks of entire third‐instar wild‐type (w1118) and NimB4sk2 larval brains stained with anti‐Draper (green) and anti‐Dcp‐1 (red). The arrows show the presence of apoptotic cells in the central area of NimB4sk2 larval brain. Scale bars = 100 μm.
  4. Quantification of caspase‐positive particles in the central brain area of larval brain. Values from at least five independent experiments are represented as mean ± SD total volume of caspase‐positive particles (**P < 0.01, by Mann–Whitney test).