MaNCP1, a C2H2 Zinc Finger Protein, Governs the Conidiation Pattern Shift through Regulating the Reductive Pathway for Nitric Oxide Synthesis in the Filamentous Fungus Metarhizium acridum.

Asexual sporulation is the most common reproduction mode of fungi. Most filamentous fungi have two conidiation patterns, normal conidiation and microcycle conidiation, which may be regulated by nutritional conditions. Nitrogen source can affect the fungal conidiation pattern, but the regulatory mechanism is not fully understood. In this study, we report a C2H2 zinc finger protein, MaNCP1, which has typical transcription factor characteristics and is screened from the subtractive library regulated by nitrate in the entomopathogenic fungus Metarhizium acridum. MaNCP1 and its N-terminal play critical roles in the conidiation pattern shift. Further study shows that MaNCP1 interacts with MaNmrA, which also contributes to the conidiation pattern shift and is involved in the reductive pathway of nitric oxide (NO) synthesis. Intriguingly, the conidiation pattern of the MaNCP1-disruption strain (ΔMaNCP1) can be restored to microcycle conidiation when grown on the microcycle conidiation medium, SYA, supplemented with NO donor or overexpressing MaNmrA in ΔMaNCP1. Here, we reveal that MaNCP1 governs the conidiation pattern shift through regulating the reductive synthesis of NO by physically targeting MaNmrA in M. acridum. This work provides new mechanistic insights into how changes in nitrogen utilization are linked to the regulation of fungal morphological changes. IMPORTANCE Fungal conidia play important roles in the response to environmental stimuli and evasion of the host immune system. The nitrogen source is one of the main factors affecting shifts in fungal conidiation patterns, but the regulatory mechanism involved is not fully understood. In this work, we report that the C2H2 zinc finger protein, MaNCP1, governs the conidiation pattern shift in M. acridum by targeting the MaNmrA gene, thereby altering the regulation of the reductive pathway for NO synthesis. This work provides further insights into how the nutritional environment can regulate the morphogenesis of filamentous fungi.

First Experimental Evidence for the Presence of Potentially Toxic Vibrio cholerae in Snails, and Virulence, Cross-Resistance and Genetic Diversity of the Bacterium in 36 Species of Aquatic Food Animals.

Vibrio cholerae is the most common waterborne pathogen that can cause pandemic cholera in humans. Continuous monitoring of V. cholerae contamination in aquatic products is crucial for assuring food safety. In this study, we determined the virulence, cross-resistance between antibiotics and heavy metals, and genetic diversity of V. cholerae isolates from 36 species of aquatic food animals, nearly two-thirds of which have not been previously detected. None of the V. cholerae isolates (n = 203) harbored the cholera toxin genes ctxAB (0.0%). However, isolates carrying virulence genes tcpA (0.98%), ace (0.5%), and zot (0.5%) were discovered, which originated from the snail Cipangopaludina chinensis. High occurrences were observed for virulence-associated genes, including hapA (73.4%), rtxCABD (68.0-41.9%), tlh (54.2%), and hlyA (37.9%). Resistance to moxfloxacin (74.9%) was most predominant resistance among the isolates, followed by ampicillin (59.1%) and rifampicin (32.5%). Approximately 58.6% of the isolates displayed multidrug resistant phenotypes. Meanwhile, high percentages of the isolates tolerated the heavy metals Hg2+ (67.0%), Pb2+ (57.6%), and Zn2+ (57.6%). Distinct virulence and cross-resistance profiles were discovered among the V. cholerae isolates in 13 species of aquatic food animals. The ERIC-PCR-based genome fingerprinting of the 203 V. cholerae isolates revealed 170 ERIC-genotypes, which demonstrated considerable genomic variation among the isolates. Overall, the results of this study provide useful data to fill gaps for policy and research related to the risk assessment of V. cholerae contamination in aquatic products.