Biology subjects

Spinti, D.

Publications and source records attributed to Spinti, D..

3 recordsLinked to original sources

bioRxiv2023

ER-anchored protein sorting controls the fate of two proteasome activators for intracellular organelle communication during proteotoxic stress

Proteotoxic stress, characterized by the accumulation of damaged proteins, poses a significant challenge to cellular homeostasis. To mitigate proteotoxicity eukaryotes employ the proteasome that is regulated by proteasome activators, e.g. transcription factors that promote gene expression of proteasome subunits. As proteotoxicity originates in different compartments, cells need to perceive signals from various locations. Understanding which components integrate signals to address proteotoxicity is essential to develop strategies to cope with proteotoxicity but remain elusive. Here, we identify that the proteasome autoregulatory feedback loop acts as a gatekeeper to facilitate the communication between nucleus and chloroplast. We reveal that the ER-anchored protein sorting system (ERAPS) controls the proteasomal degradation or nuclear translocation of proteasome activators NAC53 and NAC78. While both transcription factors activate the proteasome gene expression, they repress photosynthesis-associated nuclear genes during proteotoxicity through association with a conserved cis-element. Our data implicate a general trade-off between proteasome function and energy metabolism unravelling an unprecedented mechanism of how eukaryotic cells cope with proteotoxicity. Collectively, our discoveries provide a novel conceptual framework in which the proteasome autoregulatory feedback loop coordinates subcellular proteostasis and the trade-off between growth and defence.

plant biology↗

bioRxiv2021

The Xanthomonas type-III effector protein XopS stabilizes CaWRKY40a to regulate defense hormone responses and preinvasion immunity in pepper (Capsicum annuum)

A critical component of plant immunity against invading pathogens is the rapid transcriptional reprogramming of the attacked cell to minimize virulence. Many adapted plant bacterial pathogens use type III effector (T3E) proteins to interfere with plant defense responses, including the induction of immunity genes. The elucidation of effector function is essential to understanding bacterial pathogenesis. Here, we show that XopS, a T3E of Xanthomonas campestris pv. vesicatoria (Xcv), interacts with and inhibits the proteasomal degradation of the transcriptional regulator of defense gene expression WRKY40. Virus-induced gene silencing of WRKY40 in pepper enhanced plant tolerance towards Xcv infection, indicating it represses immunity. Stabilization of WRKY40 by XopS reduces the expression of its targets including salicylic acid (SA)-responsive genes and the jasmonic acid (JA) signaling repressor JAZ8. Xcv bacteria lacking XopS display significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by Xcv, as well as ectopic expression of XopS in Arabidopsis or Nicotiana benthamiana prevented stomatal closure in response to bacteria and biotic elicitors in a WRKY40 dependent manner. This suggests that XopS interferes with preinvasion as well as with apoplastic defense by manipulating WRKY40 stability and gene expression eventually altering phytohormone crosstalk to promote pathogen proliferation.

plant biology↗

bioRxiv2021

Self-ubiquitination of a pathogen type-III effector traps and blocks the autophagy machinery to promote disease

Beyond its role in cellular homeostasis, autophagy plays anti- and pro-microbial roles in host-microbe interactions, both in animals and plants. One prominent role of anti-microbial autophagy is to degrade intracellular pathogens or microbial molecules, in a process termed xenophagy. Consequently, microbes evolved mechanisms to hijack or modulate autophagy to escape elimination. Although well-described in animals, the extent to which xenophagy contributes to plant-bacteria interactions remains unknown. Here, we provide evidence that Xanthomonas campestris pv. vesicatoria (Xcv) suppresses host autophagy by utilizing type-III effector XopL. XopL interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection. Intriguingly, XopL is targeted for degradation by defense-related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery. Our results implicate plant antimicrobial autophagy in depletion of a bacterial virulence factor and unravels an unprecedented pathogen strategy to counteract defense-related autophagy.

plant biology↗