Carbon Catabolite Repressor UvCreA is Required for Development and Pathogenicity in Ustilaginoidea virens

The rice false smut disease, caused by Ustilaginoidea virens, has emerged as a significantglobal threat to rice production. The mechanism of carbon catabolite repression plays a crucial role in theefficient utilization of carbon nutrients and enzyme regulation in the presence of complex nutritionalconditions. Although significant progress has been made in understanding carbon catabolite repression infungi such as Aspergillus nidulans and Magnaporthe oryzae, its role in U. virens remains unclear. Toaddress this knowledge gap, we identified UvCreA, a pivotal component of carbon catabolite repression,in U. virens. Our investigation revealed that UvCreA localized to the nucleus. Deletion of UvCreA resultedin decreased growth and pathogenicity in U. virens. Through RNA-seq analysis, it was found that theknockout of UvCreA led to the up-regulation of 514 genes and down-regulation of 640 genes. Moreover,UvCreA was found to be involved in the transcriptional regulation of pathogenic genes and genesassociated with carbon metabolism in U. virens. In summary, our findings indicated that UvCreA isimportant in fungal development, virulence, and the utilization of carbon sources through transcriptionalregulation, thus making it a critical element of carbon catabolite repression.

Implications of carbon catabolite repression for plant–microbe interactions

Carbon catabolite repression(CCR)plays a key role in many physiological and adaptive responses in a broad range of microorganisms that are commonly associated with eukaryotic hosts.When a mixture of different carbon sources is available,CCR,a global regulatory mechanism,inhibits the expression and activity of cellular processes associated with utilization of secondary carbon sources in the presence of the preferred carbon source.CCR is known to be executed by completely different mechanisms in different bacteria,yeast,and fungi.In addition to regulating catabolic genes,CCR also appears to play a key role in the expression of genes involved in plant–microbe interactions.Here,we present a detailed overview of CCR mechanisms in various bacteria.We highlight the role of CCR in beneficial as well as deleterious plant–microbe interactions based on the available literature.In addition,we explore the global distribution of known regulatory mechanisms within bacterial genomes retrieved from public repositories and within metatranscriptomes obtained from different plant rhizospheres.By integrating the available literature and performing targeted meta-analyses,we argue that CCR-regulated substrate use preferences of microorganisms should be considered an important trait involved in prevailing plant–microbe interactions.

Redesigning transcription factor Cre1 for alleviating carbon catabolite repression in Trichoderma reesei

Carbon catabolite repression(CCR),which is mainly mediated by Cre1 and triggered by glucose,leads to a decrease in cellulase production in Trichoderma reesei.Many studies have focused on modifying Cre1 for alleviating CCR.Based on the homologous alignment of CreA from wild-type Penicillium oxalicum 114–2(Po-0)and cellulase hyperproducer JUA10-1(Po-1),we constructed a C-terminus substitution strain—Po-2—with decreased transcriptional levels of cellulase and enhanced CCR.Results revealed that the C-terminal domain of CreAPo−1 plays an important role in alleviating CCR.Furthermore,we replaced the C-terminus of Cre1 with that of CreAPo−1 in T.reesei(Tr-0)and generated Tr-1.As a control,the C-terminus of Cre1 was truncated and Tr-2 was generated.The transcriptional profiles of these transformants revealed that the C-terminal chimera greatly improves cellulase transcription in the presence of glucose and thus upregulates cellulase in the presence of glucose and weakens CCR,consistent with truncating the C-terminus of Cre1 in Tr-0.Therefore,we propose constructing a C-terminal chimera as a new strategy to improve cellulase production and alleviate CCR in the presence of glucose.