Tomberg, T. | bioRxiv Science

bioRxiv2025

Daily Heat Stress Induces Accumulation of Non-functional PSII-LHCII and Donor-side Limitation of PSI via Downregulation of the Cyt bf Complex in Arabidopsis thaliana

The rapidly warming climate is driving increasingly frequent and intense heat waves worldwide, posing major challenges to plant metabolism and growth. Despite the central role of photosynthesis in plant growth, the effects of prolonged heat stress on the primary reactions of photosynthesis remain poorly understood. Here, we studied how long-term heat exposure affects growth and photosynthetic performance in the model plant Arabidopsis thaliana. Plants were exposed daily to high temperature (38{degrees}C) for four hours throughout the growth period. PSII-LHCII complexes remained structurally intact, but {Delta}F/Fm, electron transfer rate (ETRII) and proportion of open reaction centers (qL) were lower under prolonged heat. Strikingly, the content of the Cytochrome b6f complex, which mediates electron transfer between photosystems, was reduced by 30-40%. Consequently, donor-side limitation of PSI was higher and the overall PSI electron transfer rate (ETRI) was lower under long-term heat. Further, carbon assimilation was significantly lower under long-term heat exposure, but PSI acceptor side limitation was not affected. We propose that downregulation of the cytochrome b6f complex restricts electron delivery to PSI, thereby preventing PSI over-reduction due to reduced carbon assimilation. Summary statementHeat-acclimated Arabidopsis thaliana plants accumulate non-functional PSII-LHCII supercomplexes. PSI complex is protected against over-reduction by restricting electron flow from Cyt b6f as an acclimatory response.

plant biology↗

bioRxiv2020

Bi-allelic variants in TSPOAP1, encoding the active zone protein RIMBP1, cause autosomal recessive dystonia

Dystonia is a debilitating hyperkinetic movement disorder, frequently transmitted as a monogenic trait. Here, we describe homozygous frameshift, nonsense and missense variants in TSPOAP1, encoding the active zone RIM-binding protein 1 (RIMBP1), as a novel genetic cause of autosomal recessive dystonia in seven subjects from three unrelated families. Subjects carrying loss-of-function variants presented with juvenile- onset progressive generalized dystonia, associated with intellectual disability and cerebellar atrophy. Conversely, subjects carrying a pathogenic missense variant (p.Gly1808Ser) presented with isolated adult-onset focal dystonia. In mice, complete loss of RIMBP1, known to reduce neurotransmission, led to motor abnormalities reminiscent of dystonia, decreased Purkinje cell dendritic arborization, and reduced numbers of cerebellar synapses. In vitro analysis of the p.Gly1808Ser variant showed larger spike-evoked calcium transients and enhanced neurotransmission, suggesting that RIMBP1-linked dystonia can be caused by either reduced or enhanced rates of spike-evoked release in relevant neural networks. Our findings establish a direct link between presynaptic RIMBP1 dysfunction and dystonia and highlight the critical role played by well-balanced neurotransmission in motor control and disease pathogenesis.

genetics↗