Table 1.

Changes due to tafazzin deficiency in the contents (mol %) of the mouse organ and human lymphoblast phospholipids (PLs) relative to the normal content of CL (mol %) in the WT or healthy individual control ((TAZ-KD_PL − WT_PL)/WT_CL or (BTHS_PL − control_PL)/control_CL).^a Numbers are shown for CL, choline (Cho), and ethanolamine (Etn) classes.

Phospholipid	Mouse				Human lymphoblast
Phospholipid	Heart	Brain	Liver	Kidney	Human lymphoblast
CL	−0.69 ± 0.06	+0.18 ± 0.67	−0.01 ± 0.21	−0.14 ± 0.11	−0.73 ± 0.05
2-MLCL	+0.38 ± 0.03	+0.16 ± 0.02	+0.17 ± 0.04	+0.27 ± 0.02	+0.64 ± 0.12
1-MLCL	+0.13 ± 0.06	+0.05 ± 0.05	+0.11 ± 0.03	+0.12 ± 0.02	+0.23 ± 0.08
Diacyl PC (with plasmanylcholine)^b	+1.21 ± 0.54	— ^c	— ^c	— ^c	— ^c
Plasmenylcholine	−1.98 ± 0.65	N.R.^d	N.R.^d	N.R.^d	N.R.^d
Diacyl PE (with plasmanylethanolamine)^b	+0.59 ± 0.25	+1.22 ± 1.81	+3.76 ± 1.45	+0.60 ± 0.66	+3.37 ± 0.79
Plasmenylethanolamine	+0.03 ± 0.08	−4.56 ± 1.76	−0.43 ± 0.24	−0.32 ± 0.22	−1.58 ± 0.96

↵a The average and error, shown as the SD, are obtained from three independent sets of biological samples (N = 3) for each of the WT and TAZ-KD mice, or healthy individuals and BTHS patients (Tables S1, S2, S3, and S4).
↵b The signal of plasmanyl glycerophospholipid as a minor component overlaps with the signal of the counterpart diacyl glycerophospholipid (Diagne et al, 1984; May et al, 1988; Kikuchi et al, 1999; Kimura et al, 2018).
↵c Content change in combination with that of plasmenylcholine is not discussed here because of a minor content of plasmenylcholine in the organ or blood cells (Diagne et al, 1984; May et al, 1988; Kikuchi et al, 1999; Kimura et al, 2018).
↵d Signal not resolved because of a minor content (Fig S1).