Biology subjects

Thordal-Christensen, H.

Publications and source records attributed to Thordal-Christensen, H..

3 recordsLinked to original sources

bioRxiv2024

A frosty genetic screen unmasks a major regulatory role for SHORT VEGETATIVE PHASE of flowering in response to a cold snap

The control of flowering in plants is intricately governed by a combination of internal and environmental signals, with temperature playing a critical role. Thus, Arabidopsis thaliana plants display temperature-dependent variations in flowering time. As unexpected periods of cold temperatures can occur at any time, plants have evolved mechanisms to detect such cold snaps and to respond by delaying flowering. Plants are more tolerant to cold temperatures in the vegetative stage, while flowers are more sensitive and have reduced reproductive success due to damage to floral structures and gametes. At the molecular level, delayed flowering can be caused by repressing the FLOWERING LOCUS T (FT) gene, and several MADS box transcription factors have been shown to repress FT expression in response to cold and in this way prevent flowering. Here, we employed a forward genetic screen aimed at understanding the effect of a cold snap on the transition to flowering. We germinated a population of A. thaliana EMS M2 plants at 20{degrees}C and then gradually lowered the temperature to 10{degrees}C and selected early flowering mutants. Using whole-genome sequencing, we identified seven mutant alleles of the SHORT VEGETATIVE PHASE (SVP) gene. This finding establishes a central role for SVP in repressing flowering in response to a cold snap and provides novel alleles, several of which affect splice junctions. Our research thus presents valuable insights into the nuanced molecular mechanisms governing temperature-responsive flowering in Arabidopsis and sheds light on the dynamic interplay between SVP and environmental cues.

plant biology↗

bioRxiv2022

Barley powdery mildew effector CSEP0162 targets multivesicular body-associated MON1 important for immunity

Encasements formed around haustoria and biotrophic hyphae as well as hypersensitive reaction (HR) cell death are essential plant immune responses to filamentous pathogens. Here we study a possible reason why these responses are absent in susceptible barley attacked by the powdery mildew fungus. We find that the effector CSEP0162 from this pathogen targets plant MON1, important for fusion of multivesicular bodies to their target membranes. Over-expression of CSEP0162 and silencing of barley MON1 both inhibit encasement formation. We find that the Arabidopsis ecotype No-0 has partial resistance to powdery mildew, and that this is dependent on MON1. Surprisingly, we find the MON1-dependent resistance in No-0 not only include an effective encasement response, but also HR. Similarly, silencing of MON1 in barley also blocked Mla3-mediated HR-based powdery mildew resistance. These data indicate that MON1 is a vital plant immunity component, and we speculate that the barley powdery mildew fungus introduces the effector CSEP0162 to target MON1 and reduce encasement formation and HR. HighlightMON1 is essential for MVB fusion to plasma membrane. We find that MON1 also is important for immunity, and that it is targeted by the barley powdery mildew effector CSEP0162.

plant biology↗

bioRxiv2022

Powdery mildew effectors AVRA1 and BEC1016 target the ER J-domain protein HvERdj3B required for immunity in barley

The barley powdery mildew fungus, Blumeria hordei (Bh), secretes hundreds of candidate secreted effector proteins (CSEPs) to facilitate pathogen infection and colonization. One of these, CSEP0008, is directly recognized by the barley nucleotide-binding leucine-rich-repeat (NLR) receptor, MLA1, and therefore designated AVRA1. Here we show that AVRA1 and the sequence-unrelated Bh effector BEC1016 (CSEP0491) suppress immunity in barley. We used yeast two-hybrid next-generation interaction screens (Y2H-NGIS), followed by binary Y2H and in planta protein-protein interactions studies, and identified a common barley target of AVRA1 and BEC1016, the endoplasmic reticulum (ER)-localized J-domain protein, HvERdj3B. Silencing of this ER quality control (ERQC) protein increased the Bh penetration. HvERdj3B is ER luminal, and we showed using split GFP that AVRA1 and BEC1016 translocate into the ER - signal peptide-independently. Silencing of HvERdj3B and expression the two effectors hampered trafficking of a vacuolar marker through the ER as a shared cellular phenotype, agreeing with the effectors targeting this ERQC component. Together, these results suggest that the barley innate immunity, preventing Bh entry into epidermal cells, is dependent on ERQC, which in turn requires the J-domain protein, HvERdj3B, regulated by AVRA1 and BEC1016. Plant disease resistance often occurs upon direct or indirect recognition of pathogen effectors by host NLR receptors. Previous work has shown that AVRA1 is directly recognized in the cytosol by the immune receptor, MLA1. We speculate that the AVRA1 J-domain target being inside the ER, where it is inapproachable by NLRs, has forced the plant to evolve this challenging direct recognition. SIGNIFICANCEThe complex plant immune system is highly dependent on fundamental cellular machineries, such as the endomembrane system and the ER quality control (ERQC), essential for delivery of immunity-associated membrane-bound and endomembrane soluble proteins to their destinations. We now find that pathogen effectors can interact with an ERQC component and suppress immunity, thereby adding to the molecular insight in plant-pathogen interactions.

plant biology↗