Javascript must be enabled to continue!
An APSES Transcription Factor Xbp1 Is Required for Sclerotial Development, Appressoria Formation, and Pathogenicity in Ciboria shiraiana
View through CrossRef
Sclerotinia diseases are important plant fungal diseases that, causes huge economic worldwide losses every year. Ciboria shiraiana is the main pathogen that results in mulberry sclerotia diseases. Sclerotia and appressoria play important roles in long-term pathogen survival and in host infection during life and disease cycles. However, the molecular mechanisms of sclerotial development and appressoria formation in C. shiraiana have not been well studied. Here, an Asm1p, Phd1p, Sok2p, Efg1p and StuAp (APSES)-type transcription factor in C. shiraiana, CsXbp1, involved in sclerotial development and appressoria formation was functionally characterized. Bioinformatics analyses showed that CsXbp1 contained an APSES-type DNA binding domain. The expression levels of CsXbp1 were higher in sclerotia and during later stages of infection. Compared with wild-type strains, hyphal growth was slower, the number and weight of sclerotia were reduced significantly, and appressoria formation was obviously delayed in CsXbp1 RNA interference (RNAi) strains. Moreover, the CsXbp1 RNAi strains showed weakened pathogenicity owing to compound appressoria defects. Tobacco rattle virus-mediated host-induced gene silencing enabled Nicotiana benthamiana to increase its resistance to C. shiraiana by reducing the CsXbp1 transcripts level. Thus, CsXbp1 plays vital roles in sclerotial formation, appressoria formation, and pathogenicity in C. shiraiana. This study provides new insights into the infection mechanisms of C. shiraiana and plant resistance breeding.
Frontiers Media SA
Title: An APSES Transcription Factor Xbp1 Is Required for Sclerotial Development, Appressoria Formation, and Pathogenicity in Ciboria shiraiana
Description:
Sclerotinia diseases are important plant fungal diseases that, causes huge economic worldwide losses every year.
Ciboria shiraiana is the main pathogen that results in mulberry sclerotia diseases.
Sclerotia and appressoria play important roles in long-term pathogen survival and in host infection during life and disease cycles.
However, the molecular mechanisms of sclerotial development and appressoria formation in C.
shiraiana have not been well studied.
Here, an Asm1p, Phd1p, Sok2p, Efg1p and StuAp (APSES)-type transcription factor in C.
shiraiana, CsXbp1, involved in sclerotial development and appressoria formation was functionally characterized.
Bioinformatics analyses showed that CsXbp1 contained an APSES-type DNA binding domain.
The expression levels of CsXbp1 were higher in sclerotia and during later stages of infection.
Compared with wild-type strains, hyphal growth was slower, the number and weight of sclerotia were reduced significantly, and appressoria formation was obviously delayed in CsXbp1 RNA interference (RNAi) strains.
Moreover, the CsXbp1 RNAi strains showed weakened pathogenicity owing to compound appressoria defects.
Tobacco rattle virus-mediated host-induced gene silencing enabled Nicotiana benthamiana to increase its resistance to C.
shiraiana by reducing the CsXbp1 transcripts level.
Thus, CsXbp1 plays vital roles in sclerotial formation, appressoria formation, and pathogenicity in C.
shiraiana.
This study provides new insights into the infection mechanisms of C.
shiraiana and plant resistance breeding.
Related Results
A eukaryote without tRNA introns
A eukaryote without tRNA introns
One of the striking characteristics of eukaryotic genomes is the presence of three types of introns: spliceosomal introns, tRNA introns, and a unique intron in the XBP1 mRNA. Excep...
Common variants in PERK , JNK , BIP and XBP1 genes are associated with the risk of prediabetes or diabetes-related phenotypes in a Chinese population
Common variants in PERK , JNK , BIP and XBP1 genes are associated with the risk of prediabetes or diabetes-related phenotypes in a Chinese population
Background
Prediabetes is an early stage of β-cell dysfunction presenting as insulin resistance. Evidences suggest that endoplasmic reticulum (ER) stress is involved in...
Nanog organizes transcription bodies
Nanog organizes transcription bodies
ABSTRACTThe localization of transcriptional activity in specialized transcription bodies is a hallmark of gene expression in eukaryotic cells. How proteins of the transcriptional m...
Predicting Thrombosis in Factor VLeiden Heterozygotes.
Predicting Thrombosis in Factor VLeiden Heterozygotes.
Abstract
Factor VLeiden (G1691A;R506Q) is an autosomal dominant allele displaying high prevalence (3–7%) in the United States Caucasian population and a high inciden...
TFinDit: transcription factor-DNA interaction data depository
TFinDit: transcription factor-DNA interaction data depository
Abstract
Background
One of the crucial steps in regulation of gene expression is the binding of transcription factor(s) to specific DNA sequences...
Function expansion of antitumor transcriptional activator NFE2L1 by the original discovery of its non-transcription factor activity
Function expansion of antitumor transcriptional activator NFE2L1 by the original discovery of its non-transcription factor activity
ABSTRACTAntitumor transcription activator NFE2L1, with the functions to regulate redox homeostasis, protein turnover, and material metabolism, plays an important role in embryonic ...
Cell Cycle–Mediated Regulation of Plant Infection by the Rice Blast Fungus
Cell Cycle–Mediated Regulation of Plant Infection by the Rice Blast Fungus
AbstractTo gain entry to plants, many pathogenic fungi develop specialized infection structures called appressoria. Here, we demonstrate that appressorium morphogenesis in the rice...
Assessing the Utility of ColabFold and AlphaMissense in Determining Missense Variant Pathogenicity for Congenital Myasthenic Syndromes
Assessing the Utility of ColabFold and AlphaMissense in Determining Missense Variant Pathogenicity for Congenital Myasthenic Syndromes
Background/Objectives: Congenital Myasthenic Syndromes (CMS) are caused by variants in >30 genes with increasing numbers of variants of unknown significance (VUS) discovered...

