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. 2023 Feb 1;24(4):e55362. doi: 10.15252/embr.202255362

Figure EV4. Differential requirements of Mi‐2 during neuronal differentiation.

Figure EV4

  1. Knockdown of Mi‐2 in adult brain neurons does not cause ectopic expression of genes. qPCR measurement of gene expression in adult heads. Mi‐2 RNAi is induced for 24 h using GAL80ts. No significant changes in expression of either vas, a10 or CG15446 were observed (one‐tailed students t‐test, represented as mean ± SEM.). Three biological replicates per genotype.
  2. Representative images of optic lobes for control and Mi‐2 knockdown in NSCs.
  3. Quantification of optic lobe neuroepithelial cells of genotypes shown in panel B (n >= 7 for each group). Represented as a box plot. No significant difference found (one‐tailed student's t‐test).
  4. Larval crawl speed (cm/min) in wor‐GAL4 × Mi‐2 RNAi and wor‐GAL4 × mCherry RNAi controls. No significant changes in crawl speed were observed (two‐tailed students t‐test, n = 10 animals per genotype). Represented as a box plot.
  5. Optic lobe phenotype is not due to Mi‐2 knockdown in glial cells. Optic lobe of third instar larvae in which repo‐GAL80 represses glial GAL4 expression. Loss of neuroepithelial cells is still observed as in elav‐GAL4; Mi‐2 RNAi brains. Scale bar = 50 μm.
  6. Characteristic rosette structure of the neuroepithelial cells is present in the control first instar optic lobe and in elav‐GAL4; Mi‐2 RNAi 1st instar optic lobes. Scale bar = 20 μm.