Global warming has been considered to accelerate the expansion of cyanobacterial blooms, which are frequently composed of the bloom-forming genera, Microcystis and Pseudanabaena, in freshwater ecosystems worldwide. Nonetheless, the impact of changes due to toxin production or lack thereof on the growth of co-existing strains, both arising from increasing temperature, has remained unknown to date. We conducted competition experiments involving toxic Microcystis PCC7806, a non-toxic mcyB⁻ mutant, and two strains of Pseudanabaena (TH-1 and DC-1) identified as P. mucicola. In mono-culture, the specific growth ratio of Pseudanabaena increased; nevertheless, the maximum cell density declined with increasing temperature. The maximum growth ratios of Pseudanabaena TH-1 and Pseudanabaena DC-1 were 0.512 day⁻¹ in the 30 °C group and 0.440 day⁻¹ in the 35 °C group, respectively. The optimum temperature for the growth of Pseudanabaena was 25 °C. Remarkably, there was no significant disparity in the maximum cell density of Microcystis PCC7806 and the mcyB⁻ mutant across varied temperature groups, even though their maximum growth rates differed marginally, reaching 0.280 day⁻¹ and 0.306 day⁻¹ in the 30 °C group, respectively. In co-cultures, the growth of Pseudanabaena TH-1 was uniformly inhibited, whereas that of DC-1 was somewhat influenced by co-culturing with toxic and non-toxic Microcystis, except for the 35 °C group, where inhibition was absent amongst DC-1 and Microcystis. Moreover, the growth of Microcystis was promoted with a co-culture of TH-1 in the 20 °C groups. Conversely, the co-culture of Microcystis with Pseudanabaena DC-1 led to the inhibition of the former in the 30 °C and 35 °C groups. With a Lotka–Volterra competition model, the results showed that Microcystis dominated or co-existed with Pseudanabaena, conforming to expectations from the wild.

Introduction. Distal arthrogryposis type 5D (DA5D) is an autosomal recessive disease. The clinical symptoms include contractures of the joints of limbs, especially camptodactyly of the hands and/or feet, unilateral ptosis, a round‐shaped face, arched eyebrows, and micrognathia, without ophthalmoplegia. ECEL1 is a DA5D causative gene that encodes a membrane‐bound metalloprotease. ECEL1 plays important roles in the final axonal arborization of motor nerves in limb skeletal muscles and neuromuscular junction formation during prenatal development. Methods. A DA5D family with webbing of the elbows and fingers was recruited. We performed whole‐exome sequencing (WES) and filtered mutations by disease‐causing genes of arthrogryposis multiplex congenita (AMC). Mutational analysis and cosegregation confirmation were then performed. Results. We identified novel compound heterozygous mutations of ECEL1 (NM_004826: c.69C>A, p.C23∗ and c.1810G>A, p.G604R) in the proband. Conclusions. We detected causative mutations in a DA5D family, expanding the spectrum of known ECEL1 mutations and contributing to the clinical diagnosis of DA5D.