Photosystem II (PSII) is the multi-subunit light-driven oxidoreductase that drives photosynthetic electron transport using electrons extracted from water. To investigate the initial steps of PSII assembly, we used strains of the cyanobacterium Synechocystis sp. PCC 6803 arrested at early stages of PSII biogenesis and expressing affinity-tagged PSII subunits to isolate PSII reaction center assembly (RCII) complexes and their precursor D1 and D2 modules (D1_mod and D2_mod). RCII preparations isolated using either a His-tagged D2 or a FLAG-tagged PsbI subunit contained the previously described RCIIa and RCII* complexes that differ with respect to the presence of the Ycf39 assembly factor and high light-inducible proteins (Hlips) and a larger complex consisting of RCIIa bound to monomeric PSI. All RCII complexes contained the PSII subunits D1, D2, PsbI, PsbE, and PsbF and the assembly factors rubredoxin A and Ycf48, but we also detected PsbN, Slr1470, and the Slr0575 proteins, which all have plant homologs. The RCII preparations also contained prohibitins/stomatins (Phbs) of unknown function and FtsH protease subunits. RCII complexes were active in light-induced primary charge separation and bound chlorophylls (Chls), pheophytins, beta-carotenes, and heme. The isolated D1_mod consisted of D1/PsbI/Ycf48 with some Ycf39 and Phb3, while D2_mod contained D2/cytochrome b₅₅₉ with co-purifying PsbY, Phb1, Phb3, FtsH2/FtsH3, CyanoP, and Slr1470. As stably bound, Chl was detected in D1_mod but not D2_mod, formation of RCII appears to be important for stable binding of most of the Chls and both pheophytins. We suggest that Chl can be delivered to RCII from either monomeric Photosystem I or Ycf39/Hlips complexes.

Microbes in marine ecosystems are known to produce secondary metabolites. One of which are carotenoids, which have numerous industrial applications, hence their demand will continue to grow. This review highlights the recent research on natural carotenoids produced by marine microorganisms. We discuss the most recent screening approaches for discovering carotenoids, using in vitro methods such as culture-dependent and culture-independent screening, as well as in silico methods, using secondary metabolite Biosynthetic Gene Clusters (smBGCs), which involves the use of various rule-based and machine-learning-based bioinformatics tools. Following that, various carotenoids are addressed, along with their biological activities and metabolic processes involved in carotenoids biosynthesis. Finally, we cover the application of carotenoids in health and pharmaceutical industries, current carotenoids production system, and potential use of synthetic biology in carotenoids production.

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Context: Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, highlighting the need for novel targeted therapies. Clitoria ternatea (CT), a medicinal plant with diverse bioactive compounds, shows promising anticancer potential in preclinical studies, yet its molecular mechanisms in CRC remain poorly understood. Aims: To elucidate the anti-CRC mechanisms and potential therapeutic targets of CT compounds through integrated bioinformatics and network pharmacology approaches. Methods: Active CT compounds were obtained from the literature and screened for drug-likeness. CRC-associated targets from GeneCards were intersected with CT-related targets to identify overlapping candidates. Overlapping targets were analyzed using network pharmacology, Gene Ontology (GO), and KEGG pathway enrichment. Hub genes were validated through mRNA expression, pathological stage correlations, and molecular docking, followed by 100-ns molecular dynamics simulations to assess binding stability. Results: Thirty-two CT compounds and eleven potential CRC-related targets were identified, with CCND1 and HSP90AB1 emerging as central hub genes linked to the PI3K/AKT and CRC signaling pathways. Ellagic acid exhibited the strongest binding affinity to CCND1 (−8.3 kcal/mol) and HSP90AB1 (−9.5 kcal/mol), and maintained conformational stability during simulations, outperforming control ligands. These findings highlight the multi-target therapeutic potential of CT in CRC. Further in vitro studies are needed to investigate CCND1 and HSP90AB1 expression, cell proliferation, and apoptosis in CRC models. Conclusions: CT exhibits multi-target anti-CRC potential by modulating CCND1 and HSP90AB1, suggesting a mechanistic link to the PI3K/AKT signaling pathway. These results support further validation (in vitro and in vivo studies) of CT and ellagic acid as potential adjuvant CRC therapies.