Biology subjects

Bindics, J.

Publications and source records attributed to Bindics, J..

5 recordsLinked to original sources

bioRxiv2023

Tip of the iceberg? Three novel TOPLESS interacting effectors of the gall-inducing fungus Ustilago maydis

O_LIUstilago maydis is a biotrophic pathogen causing smut disease in maize. It secretes a cocktail of effector proteins during its biotrophic stages in the host plant, which target different host proteins. One such class of proteins we identified previously is TOPLESS (TPL) and TOPLESS RELATED (TPR) transcriptional corepressors. C_LIO_LIHere we screen 297 U. maydis effector candidates for their ability to interact with maize TPL protein RAMOSA 1 ENHANCER LOCUS 2 Like 2 (RELK2) and their ability to induce auxin signaling and thereby identified three novel TPL /TPR interacting effector proteins (Tip6, Tip7 and Tip8). Two of them, Tip6 and Tip7 contain a classical ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motif and interact with maize TPL protein RELK2 in nuclear compartments, whereas Tip8 lacks known TPL interaction motifs and its overexpression in non-host plant leads to cell death indicating recognition of the effector. C_LIO_LIBy using structural modeling, we show an interaction of Tip6 and Tip7 with the previously crystallized EAR motif binding domain of RELK2. Furthermore, by infection assays with an octuple deletion mutant of U. maydis, we demonstrate a role of Tips in U. maydis virulence. Our findings suggest the TOPLESS class of corepressors as a major hub of U. maydis effector proteins. C_LI

plant biology↗

bioRxiv2022

Composition can buffer protein dynamics within liquid-like condensates.

Most non-membrane-bound compartments in cells that form via phase separation have complex composition. While phase separation of individual proteins that form these compartments is well-documented, the mechanisms that modulate dynamics of individual proteins in multicomponent systems remain unclear. Here, we used in vitro reconstitution and in vivo experiments to investigate how the dynamics of a scaffold protein PGL-3 is regulated within the liquid-like P granule compartment in C. elegans. Using mutational and biophysical perturbations, we generated PGL-3 constructs that form condensates in vitro with widely varying dynamics. Using these PGL-3 constructs, we show that introducing other P granule components buffers against change of dynamics within liquid-like condensates. This dynamics-buffering effect is mediated by weak interactions among two or more components. Such dynamics-buffering may contribute to robust functional output of cellular liquid-like compartments.

cell biology↗

bioRxiv2021

TOPLESS promotes plant immunity by repressing auxin signaling and is targeted by the fungal effector Naked1

In plants, the antagonism between growth and defense is hardwired by hormonal signaling. Perception of Pathogen Associated Molecular Patterns (PAMPs) from invading microorganisms inhibits auxin signaling and growth. Conversely, pathogens manipulate auxin signaling to promote disease, but how this hormone inhibits immunity is not fully understood. Ustilago maydis is a maize pathogen that induces auxin signaling in its host. We characterized an U. maydis effector protein, Naked1 (Nkd1), that is translocated into the host nucleus. Through its native EAR motif, Nkd1 binds to the transcriptional co-repressors TOPLESS/TOPLESS related (TPL/TPRs) and prevents the recruitment of transcriptional repressors involved in hormonal signaling, leading to de-repression of auxin and jasmonate signaling. Moderate up-regulation of auxin signaling inhibits an early defense response, PAMP-triggered ROS burst. Thus, our findings establish a clear mechanism for auxin-induced pathogen susceptibility. Manipulation of TPL by Nkd1 is evolutionary well balanced as engineered Nkd1 variants with increased expression or increased EAR-mediated TPL/TPR binding trigger typical salicylic acid mediated defense reactions, leading to pathogen resistance.

plant biology↗

bioRxiv2019

Fungal effector Jsi1 hijacks plant JA/ET signaling through Topless

Ustilago maydis (U. maydis) is the causal agent of maize smut disease. During the colonization process, the fungus secretes effector proteins which suppress immune responses and redirect the host-metabolism in favor of the pathogen. Here we describe a novel strategy by which U. maydis induces plant jasmonate/ethylene (JA/ET) hormone signaling and thereby biotrophic susceptibility. The U. maydis effector Jasmonate/Ethylene signaling inducer 1 (Jsi1) possesses an ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motif, DLNxxP, which interacts with the second WD40 domain of the conserved plant co-repressor family Topless/Topless related (TPL/TPR). Jsi1 interaction with TPL/TPRs leads to derepression of the ethylene response factor (ERF) branch of the JA/ET signaling pathway, supporting biotrophic susceptibility. Jsi1 likely activates the ERF branch by interfering with the binding of endogenous DLNxxP motif-containing ERF transcription factors to TPL/TPR proteins. The identification of effector proteins possessing a DLNxxP motif in different fungal species with biotrophic and hemibiotrophic lifestyles together with the validation of the interaction between such effectors from Magnaporthe oryzae (M. oryzae), Sporisorium scitamineum (S. scitamineum), and S. reilianum with TPL proteins indicates the convergent evolution of effectors for modulating the TPL/TPR co-repressor hub.

plant biology↗

bioRxiv2019

The Pleiades cluster of fungal effector genes inhibit 1 host defenses

SummaryBiotrophic plant pathogens secrete effector proteins to manipulate the host physiology. Effectors suppress defenses and induce an environment favorable to disease development. Sequence-based prediction of effector function is difficulted by their rapid evolution rate. In the maize pathogen Ustilago maydis, effector-coding genes frequently organize in clusters. Here we describe the functional characterization of the pleiades, a cluster of ten symplastic effectors. Deletion of the pleiades leads to strongly impaired virulence and accumulation of reactive oxygen species (ROS) in infected tissue. Eight of the Pleiades suppress the production of ROS upon perception of pathogen associated molecular patterns (PAMPs). Although genetically redundant, the Pleiades target different host components. The paralogs Taygeta1 and Merope1 suppress ROS production in either the cytoplasm or nucleus, respectively. Merope1 targets and promotes the autoubiquitination activity of RFI2, a conserved family of E3 ligases that regulates the production of PAMP-triggered ROS burst and influences flowering time in plants.

microbiology↗