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.

Gonadotropin-inhibitory hormone (GnIH) is a neuropeptide involved in the regulation of reproductive function in vertebrates. It is able to inhibit the synthesis and secretion of GnRH and Gth in the HPG axis. However, the regulatory role and mechanism by which current gonadal steroid hormones regulate GnIH are still unclear. In this study, transcription factor binding site analysis was performed on the promoter sequence of zebrafish GnIH. Whereafter, transgenic zebrafish (GnIH: mCherry) accurately labeled GnIH and esr2b knockout zebrafish, which were constructed previously, were used to explore the regulation between estrogen and GnIH. In vitro exposure of wild-type zebrafish embryos and transgenic zebrafish embryos to estradiol showed that 10 μM estradiol significantly increased the transcription level of GnIH. However, both 10 μM and 50 μM estradiol significantly increased the transcription level of GnIH in esr2b knockout zebrafish. We compared the expression levels of GnIH in esr2b knockout zebrafish and wild-type zebrafish at different developmental stages (48 hpf–120 hpf). The results showed that from 96 hpf, the expression level of GnIH in esr2b knockout zebrafish was significantly higher than that in wild-type zebrafish, indicating that esr2b is involved in the negative regulation of GnIH, and this regulatory relationship is established on the fourth day of zebrafish development.