The effects of temperature and sulfamethoxazole on the growth and photosynthetic characteristics of Phaeodactylum tricornutum.

The misuse of antibiotics has brought potential ecological risks to marine ecosystems, especially under a changing climate. Laboratory experiments were conducted to understand the impact of rising temperatures and antibiotic sulfamethoxazole (SMX) abuse on marine diatom Phaeodactylum tricornutum. Temperatures of 21 and 24 °C were optimal for the growth and photosynthetic characteristics of P. tricornutum. When exposed to higher temperatures (≥27 °C), the growth and photosynthesis were inhibited. High concentrations of SMX (≥100 mg/L) caused rapid and acute toxicological effects on the phytoplankton. In contrast, low concentrations of SMX (1 mg/L) exhibited hormesis. When P. tricornutum was exposed to SMX at high temperatures, the stress on the phytoplankton was even more pronounced. This suggests that the combination of rising temperatures and antibiotic pollution may have a more significant negative impact on marine phytoplankton than either stressor alone. Neglecting the interaction between these stressors may lead to underestimating their combined effects on marine ecosystems.

Osa-miR164a targets OsNAC60 and negatively regulates rice immunity against the blast fungus Magnaporthe oryzae.

Exploring the regulatory mechanism played by endogenous rice miRNAs in defense responses against the blast disease is of great significance in both resistant variety breeding and disease control management. We identified rice defense-related miRNAs by comparing rice miRNA expression patterns before and after Magnaporthe oryzae strain Guy11 infection. We discovered that osa-miR164a expression reduced upon Guy11 infection at both early and late stages, which was perfectly associated with the induced expression of its target gene, OsNAC60. OsNAC60 encodes a transcription factor, over-expression of which enhanced defense responses, such as increased programmed cell death, greater ion leakage, more reactive oxygen species accumulation and callose deposition, and upregulation of defense-related genes. By using transgenic rice over-expressing osa-miR164a, and a transposon insertion mutant of OsNAC60, we showed that when the miR164a/OsNAC60 regulatory module was dysfunctional, rice developed significant susceptibility to Guy11 infection. The co-expression of OsNAC60 and osa-miR164a abolished the OsNAC60 activity, but not its synonymous mutant. We further validated that this regulatory module is conserved in plant resistance to multiple plant diseases, such as the rice sheath blight, tomato late blight, and soybean root and stem rot diseases. Our results demonstrate that the miR164a/OsNAC60 regulatory module manipulates rice defense responses to M. oryzae infection. This discovery is of great potential for resistant variety breeding and disease control to a broad spectrum of pathogens in the future.

Magnaporthe oryzae Induces the Expression of a MicroRNA to Suppress the Immune Response in Rice.

MicroRNAs play crucial roles in plant responses to pathogen infections. The rice blast disease, caused by the fungus Magnaporthe oryzae, is the most important disease of rice (Oryza sativa). To explore the microRNA species that participate in rice immunity against the rice blast disease, we compared the expression of small RNAs between mock- and M. oryzae-treated rice. We found that infection by M. oryzae strain Guy11 specifically induced the expression of rice miR319 and, consequently, suppressed its target gene TEOSINTE BRANCHED/CYCLOIDEA/PROLIFERATING CELL FACTOR1 (OsTCP21), which encodes a transcription factor. Using transgenic rice that overexpresses miR319b (OE) or expresses OsTCP21-Res (which is resistant to miR319-mediated silencing), we found that OsTCP21 is a positive regulator of the rice defense response against the blast disease. When wild-type and miR319b-OE rice were infected by Guy11, multiple jasmonic acid (JA) synthetic and signaling components were suppressed, indicating that Guy11 suppresses JA signaling through inducing miR319. In particular, we found that LIPOXYGENASE2 (LOX2) and LOX5 were specifically suppressed by miR319 overexpression or by Guy11 infection. LOXs are the key enzymes of JA synthesis, which catalyze the conversion of α-linoleic acid to hydroperoxy-octadecadienoic acid. The application of α-linoleic acid rescued disease symptoms on the OsTCP21-Res rice but not wild-type rice, supporting our hypothesis that OsLOX2 and OsLOX5 are the key JA synthesis genes hijacked by Guy11 to subvert host immunity and facilitate pathogenicity. We propose that induced expression of OsLOX2/5 may improve resistance to the rice blast disease.