Extended Data Figure 7: Zinc-fingers are essential for neurogenic function of Myt1l.
From: Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates
a, Schematic of Myt1l zinc-finger 2–3 point and deletion mutants. The ability to enhance neurogenic conversion together with Ascl1 is indicated by (+), non-functional mutants are indicated with (−) (see also Fig. 3). b, Sequence alignments and conservation of CCHC-type zinc-fingers from Myt1l; cysteine and histidine residues that can coordinate Zn(II) are highlighted in purple, non-coordinating mutated histidines are shown in green. c, Representative immunofluorescence of iN cells derived from MEFs upon reprogramming for 14 days with Ascl1 and the indicated transgenes; TUJ1 (red), DAPI staining (blue), scale bar, 50 μm. d–h, Electrophysiological characterization of iN cells derived in c upon maturation for 21 days on mouse glia. d, Representative action potential (AP) traces of iN cells generated with indicated transgenes; pie charts indicate fraction of cells firing single (grey), multiple (white), or no (black) action potentials. e, Mean number of action potentials fired plotted with respect to pulse amplitude measured at −60 mV holding potential. f, Mean resting membrane potential (Vrest). g, h, Mean membrane resistance (Rm; g) and capacitance (Cm; h) measured at −70 mV holding potential. Dotted line indicates intrinsic properties of Ascl1 + wild-type Myt1l or Ascl1 + Myt1l200–912 cells; n = 3 biological replicates (total number of individual cells measured indicated), error bars show s.e.m., t-test *P < 0.05.
