PMC

a) Plot displaying normalized driver diversity and driver prevalence (fraction of tumor samples mutated) for driver missense mutations in 32 cancer types. K-means clustering identified 5 clusters with centroids shown as numerically designated circles. b) Prevalence of driver missense mutations identified by CHASMplus as a function of sample size. Lines represent LOWESS fit to different rarities of driver missense mutations. TCGA acronyms for cancer types are listed in the Methods.

Outcome by whether driver mutations are clonal or subclonal. Leukemia-free survival for patients showing no mutation (gray), clonal driver mutations (blue), or subclonal driver mutations (red) for (A) TET2, (B) ASXL1, (C) SRSF2, (D) EZH2, (E) CBL, and (F) RUNX1. The P values denote the hypothesis test of whether splitting driver mutations into clonal or subclonal categories improves fit in a Cox proportional hazards model.

Blocking synaptic ACh release from L4 neurons leads to slow repolarization in LMCs. A, ERG recording traces of L4-GAL4/UAS-vAChT^RNAi and UAS-vAChT^RNAi/+ flies. Right, Quantification of the time (t_1/4) required for a 1/4 recovery and the number of recorded flies. B, ERG recording traces of the flies with expression of TeTxLC using L4-GAL4 driver. Event markers represent 5 s orange light pulses. Calibration: ERG traces throughout all figures, 5 mV. C, The decay of ERG recordings in WT and L4-Gal4/UAS-TeTxLC flies is fit with double or single exponential decay fit, respectively. Solid lines indicate the averaged experimental ERG recording decay traces. Dashed lines indicate the exponential decay fit. w¹¹¹⁸: R² = 99.45%; L4-Gal4/UAS-TeTxLC: R² = 99.72%. Arrows indicate decay constants for the fast and slow component of the exponential. D, Quantification of the time (t_1/4) required for a 1/4 recovery from the responses on stimulation cessation and the number of recorded flies for each genotype. E, ERG recording traces of the flies with expression of hid, or Kir2.1 using L4-GAL4 driver. Event markers represent 5 s orange light pulses. Calibration: ERG traces throughout all figures, 5 mV. Right, Quantification of the time (t_1/4) required for a 1/4 recovery from the responses on stimulation cessation and the number of recorded flies for each genotype. F, Intracellular recording represents slow repolarization in L4-GAL4/UAS-TeTxLC LMCs. Event markers represent 200 ms light pulses. Calibration: intracellular recording traces, 2.5 mV. Top, Measurements of the amplitude (Am) and rise time (Rt) of light-induced hyperpolarization. G, The decay of intracellular recordings in LMCs are fit with single exponential decay fit. Solid lines indicate the averaged decay trace of experimental intracellular recording. Dashed lines indicate the single exponential decay fit. w¹¹¹⁸: R² = 98.72%; L4-Gal4/UAS-TeTxLC: R² = 98.52%. Arrows indicate decay constants for the exponential fit. H, Intracellular recording reveals normal light response in w¹¹¹⁸ and L4-GAL4/UAS-TeTxLC photoreceptors. Event markers represent 5 s orange light pulses. Calibration: intracellular recording traces, 5 mV. I, The decay of intracellular recordings in photoreceptor cells are fit with double exponential decay fit. Solid lines indicate the averaged decay trace of experimental intracellular recording. Dashed lines indicate the exponential decay fit. w¹¹¹⁸: R² = 91.43%; L4-Gal4/UAS-TeTxLC: R² = 73.21%. Arrows indicate decay constants for the fast component of the exponential fit. **p < 0.01. ***p < 0.001.

LED driver has been compared to a laser diode on a FLIM measurement. ICG in water and DMSO have been measured and lifetime difference differed on average by 3.6% between the two light sources. The experimental data have been fit to sinewaves with correlations greater then 98% for the LED driver and 99% for the laser diode. Results are plotted normalized to the depth-of-modulation of the fluorescence data form the laser diode.