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Photosynthetic organisms have to tolerate rapid changes in light intensity, which is facilitated by non-photochemical quenching (NPQ) and involves modification of energy transfer from light-harvesting complexes (LHC) to the photosystem reaction centres. NPQ includes dissipating excess light energy to heat (qE) and the reversible coupling of LHCII to photosystems (state transitions/qT), which are considered separate NPQ mechanisms. In the model alga  Chlamydomonas reinhardtii  the LHCSR3 protein has a well characterised role in qE. Here, it is shown in the  npq4  mutant, deficient in LHCSR3, that energy coupling to photosystem II (PSII) more akin to qT is also disrupted, but no major differences in LHC phosphorylation or LHC compositions were found in comparison to wild-type cells. The qT of wild-type cells possessed two kinetically distinguishable phases, with LHCSR3 participating in the more rapid (<2 min) phase. This LHCSR3-mediated qT was sensitive to physiological levels of H 2 O 2 , which accelerated qE induction, revealing a way that may help  C. reinhardtii  tolerate a sudden increase in light intensity. Overall, a clear mechanistic overlap between qE and qT is shown.

LHCSR3 affects de-coupling and re-coupling of LHCII to PSII during state transitions in Chlamydomonas reinhardtii