bims-plasge 2025-04-20 papers

Issue of 2025–04–20
two papers selected by
Vera S. Bogdanova, ИЦиГ СО РАН

Curr Biol. 2025 Apr 15. pii: S0960-9822(25)00392-6. [Epub ahead of print]

Hijacking and integration of algal plastids and mitochondria in a polar planktonic host.

Ananya Kedige Rao, Daniel Yee, Fabien Chevalier, Charlotte LeKieffre, Marie Pavie, Marine Olivetta, Omaya Dudin, Benoit Gallet, Elisabeth Hehenberger, Mehdi Seifi, Florian Jug, Joran Deschamps, Ting-Di Wu, Rebecca Gast, Pierre-Henri Jouneau, Johan Decelle.

In oceanic plankton, various hosts are capable of engulfing and temporarily integrating microalgae (photosymbiosis) or just their photosynthetic plastids (kleptoplastidy) from the environment. These cellular interactions have been hypothesized to be representative of evolutionary steps in plastid acquisition in eukaryotes, but the underlying mechanisms are not fully understood. Here, we studied a polar kleptoplastidic dinoflagellate, which is known to steal plastids of the microalga Phaeocystis antarctica. We tracked the morphology and activity of stolen plastids over several months by combining multimodal subcellular imaging and photophysiology. Upon integration inside a host vacuole, the volume of plastids and pyrenoids significantly increased, and photosynthetic activity was boosted. This may be supported by the retention of a 50-fold larger algal nucleus for ∼1 week. Once the algal nucleus was lost, there was a decrease in plastid volume and photosynthesis, but nucleus- and plastid-encoded photosystem subunits were still detected. Carbon fixation and transfer to the host were also maintained after >2 months. We also showed that the algal mitochondrion was stolen and retained for several months, transforming into an extensive network interacting with plastids. This highlights a complex strategy in plankton along the continuum of plastid symbioses, where both plastids and mitochondria of a microalga are hijacked by a host for several months without the algal nucleus. This association, which we found to be widely distributed in polar regions, suggests that plastid-mitochondrion interaction may have played a role in the evolution of plastid acquisition and opens new questions about host control and organelle maintenance.

Keywords: 3D electron microscopy; dinoflagellate; kleptoplastidy; marine plankton; microalga; mitochondria; photosynthesis; plastid; symbiosis

DOI: https://doi.org/10.1016/j.cub.2025.03.076

Cell Calcium. 2025 Apr 08. pii: S0143-4160(25)00026-0. [Epub ahead of print]127 103017

Calcium acts as a critical determinant of mitochondria-nuclear networking driven retrograde signaling.

Kriti Ahuja, Rajender K Motiani.

Mitochondria are robust signaling organelle that regulate a variety of cellular functions. One of the key mechanisms that drive mitochondrial signaling is inter-organelle crosstalk. Mitochondria communicates with other organelles primarily via exchange of calcium (Ca2+), reactive oxygen species (ROS) and lipids across organelle membranes. Mitochondria has its own genome but a majority of mitochondrial proteins are encoded by nuclear genome. Therefore, several mitochondrial functions are controlled by nucleus via anterograde signaling. However, the role of mitochondria in driving expression of genes encoded by nuclear genome has recently gained attention. Recent studies from independent groups have demonstrated a critical role for mitochondrial Ca2+signaling in stimulating nuclear gene expression. These studies report that inhibition of mitochondrial Ca2+uptake through silencing of Mitochondrial Ca2+Uniporter (MCU) leads to Ca2+oscillations in the cytosol. The rise in cytosolic Ca2+ results in activation of Ca2+ sensitive transcription factors such as NFATs and NF-κB. These transcription factors consequently induce expression of their target genes in the nuclear genome. It is important to highlight that these groups used different cell types and elegantly presented a phenomenon that is conserved across various systems. Notably, mitochondrial Ca2+ signaling mediated transcriptional regulation controls diverse cellular functions ranging from B-cell activation, melanogenesis and aging associated inflammation. Future studies on this signaling module would result in better understanding of this axis in human pathophysiology and could lead to development of novel therapeutic strategies.

Keywords: Calcium sensitive transcription factors; Mitochondrial calcium signaling; Nuclear transcription; Retrograde signaling

DOI: https://doi.org/10.1016/j.ceca.2025.103017