4.8 Article

Parasitic modulation of host development by ubiquitin-independent protein degradation

Journal

CELL
Volume 184, Issue 20, Pages 5201-+

Publisher

CELL PRESS
DOI: 10.1016/j.cell.2021.08.029

Keywords

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Funding

  1. Human Frontier Science Program [RGP0024/2015]
  2. Marie Curie International Incoming Fellowship FP7-PEOPLE-2010-IIF grant [274444]
  3. Biotechnology and Biological Sciences Research Council [BBS/E/J/000PR9797]
  4. John Innes Foundation
  5. Academia Sinica

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This study demonstrates how SAP05 protein effectors from insect-vectored plant pathogenic phytoplasmas control several plant developmental processes by prolonging host lifespan and inducing witches' broom-like proliferations of leaf and sterile shoots. These effectors act by mediating the concurrent degradation of SPL and GATA developmental regulators via a process that relies on hijacking the plant ubiquitin receptor RPN10.
Certain obligate parasites induce complex and substantial phenotypic changes in their hosts in ways that favor their transmission to other trophic levels. However, the mechanisms underlying these changes remain largely unknown. Here we demonstrate how SAP05 protein effectors from insect-vectored plant pathogenic phytoplasmas take control of several plant developmental processes. These effectors simultaneously prolong the host lifespan and induce witches' broom-like proliferations of leaf and sterile shoots, organs colonized by phytoplasmas and vectors, SAP05 acts by mediating the concurrent degradation of SPL and GATA developmental regulators via a process that relies on hijacking the plant ubiquitin receptor RPN10 independent of substrate ubiquitination. RPN10 is highly conserved among eukaryotes, but SAP05 does not bind insect vector RPN10. A two-amino-acid substitution within plant RPN10 generates a functional variant that is resistant to SAP05 activities. Therefore, one effector protein enables obligate parasitic phytoplasmas to induce a plethora of developmental phenotypes in their hosts.

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