Spirogyra filaments show unique photomovement that differs in response to blue, red, and far‐red light. Phototropins involved in the blue‐light movement have been characterized together with downstream signaling components, but the photoreceptors and mechanical effectors of red‐ and far‐red light movement are not yet characterized. The filaments of Spirogyra varians slowly bent and aggregated to form a tangled mass in red light. In far‐red light, the filaments unbent, stretched rapidly, and separated from each other. Mannitol and/or sorbitol treatment significantly inhibited this far‐red light movement suggesting that turgor pressure is the driving force of this movement. The bending and aggregating movements of filaments in red light were not affected by osmotic change. Three phytochrome homologues isolated from S. varians showed unique phylogenetic characteristics. Two canonical phytochromes, named SvPHY1 and SvPHY2, and a noncanonical phytochrome named SvPHYX2. SvPHY1 is the first PHY1 family phytochrome reported in zygnematalean algae. The gene involved in the transport of phytochromes into the nucleus was characterized, and its expression in response to red and far‐red light was measured using quantitative PCR. Our results suggest that the phytochromes and the genes involved in the transport system into the nucleus are well conserved in S. varians.

In many filamentous red algae, cells that die from physical damage are replaced through somatic fusion of repair cells formed from adjacent cells. We visualized ROS generation in repair cells of Giriffthsia monilis using DCFH-DA staining and examined the expression of the genes involved in wound healing using quantitative PCR. Repair cells elongate along the H2O2 gradient, meet at each other’s tips where the H2O2 concentration is highest, and undergo somatic fusion. No wound response occurred with ascorbic acid treatment. Conversely, H2O2 treatment induced many repair cells, leading to multiple somatic cell fusions. Diphenylene iodonium (DPI) or caffeine treatment reversibly inhibited ROS production in repair cells and blocked the progression of the wound response suggesting that ROS and calcium signaling are involved in the process. Four G. monilis homologues of NADPH-oxidase (GmRBOHs) were identified. The expression of GmRBOHs was upregulated upon injury, peaking 1 h post injury, and decreasing to initial levels when repair cells began to elongate. Our results suggest that ROS generated upon cell injury activates Ca2+ channels and upregulates the expression of GmRBOHs, and that H2O2 generated from repair cells mediates induced repair cell elongation leading to somatic cell fusion and filament repair.