Finding. Chlamydomonas NADK2 is a commuting NAD kinase. In the light it lives mostly in the chloroplast. In the dark, on acetate, more of it sits in mitochondria. Delete it and mitochondrial NADP(H) falls, the TCA cycle stalls, and heterotrophic growth nearly stops. Turn the lights on and chloroplast NADK1 plus a glyoxylate-shunt detour around TCA let the mutant grow, while mitochondrial ROS drops. Location is the regulation.
Why this paper matters
NADP(H) is compartmental. A kinase that changes address with trophic mode is a cleaner demonstration than another static dual-target blot. The dark-growth collapse is the necessity proof. The light workaround is the metabolic-flexibility proof.
Human readers must not confuse CreNADK2 with human NADK2, which is already mitochondrial. The logic still transfers: if you cannot make mitochondrial NADP, TCA-dependent lifestyles fail.
What they actually measured
Isoform localization under three growth modes. nadk2 mutant NADP(H), TCA, heterotrophic growth. Light rescue via NADK1 and glyoxylate rerouting, with lower mitochondrial ROS.
How to read the score
Around 80. Dual targeting, conditionality, TCA, ROS, and a bypass. Confidence is medium-high for the alga. Score 81.
What to do with it
If you work on NADP compartments, algal heterotrophy, or TCA versus glyoxylate, pull the localization splits and the dark-growth curves. Do not annotate human NADK2 from this paper’s numbering. The directional implication is that mitochondrial NADP supply is optional in the light and obligatory in the dark, and the kinase moves to match.