Manipulation of plant cells by cyst and root-knot nematode effectors.
A key feature of sedentary plant-parasitic nematodes is the release of effector proteins from their esophageal gland cells through their stylets into host roots. These proteinaceous stylet secretions have been shown to be crucial for successful parasitism by mediating the transition of normal root cells into specialized feeding sites and by negating plant defenses. Recent technical advances of purifying mRNA from esophageal gland cells of plant-parasitic nematodes coupled with emerging sequencing technologies is steadily expanding our knowledge of nematode effector repertoires. Host targets and biological activities of a number of nematode effectors are continuously being reported and, by now, a first picture of the complexity of sedentary nematode parasitism at the molecular level is starting to take shape. In this review, we highlight effector mechanisms that recently have been uncovered by studying the host-pathogen interaction. These mechanisms range from mediating susceptibility of host plants to the actual triggering of defense responses. In particular, we portray and discuss the mechanisms by which nematode effectors modify plant cell walls, negate host defense responses, alter auxin and polyamine signaling, mimic plant molecules, regulate stress signaling, and activate hypersensitive responses. Continuous molecular characterization of newly discovered nematode effectors will be needed to determine how these effectors orchestrate host signaling pathways and biological processes leading to successful parasitism.
Department of Plant pathology and Microbiology, Iowa State University, Ames, IA, USA.
Tarek
T
Hewezi
Thomas J
TJ
Baum
D000818:Animals; D006790:Host-Parasite Interactions / Q000235:genetics*; D010935:Plant Diseases / Q000276:immunology / Q000469:parasitology*; D057865:Plant Immunity; D018517:Plant Roots / Q000469:parasitology; D010944:Plants / Q000235:genetics / Q000469:parasitology*; D015398:Signal Transduction; D014431:Tylenchoidea / Q000235:genetics / Q000502:physiology*