FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2009738587> ?p ?o ?g. }

• W2009738587 endingPage "575" @default.
• W2009738587 startingPage "571" @default.
• W2009738587 abstract "Parasitic plants can severely retard the growth and productivity of their host plants, and those that have shifted from their ancestral hosts to commercial crops are now a severe obstacle to agriculture, causing crop losses that amount to billions of dollars annually (Parker, 2009). For example, species of the genus Orobanche (broomrapes) that have shifted to commercial crops are now a major constraint to agriculture in many parts of the world, particularly in the Mediterranean. Research into the host–parasite interface has mushroomed in recent decades, and Orobanche has become a model for understanding host plant resistance at the cellular (Goldwasser et al., 2000; Zehhar et al., 2003; Pérez-de-Luque et al., 2005b, 2006, 2008) and molecular levels (Joel & Portnoy, 1998; Letousey et al., 2007; Hiraoka et al., 2009). However, host plant resistance mechanisms are multifaceted, complex and vary between host species (Serghini et al., 2001; Rubiales, 2003; Labrousse et al., 2004), and the complexity of the Orobanche–host plant interaction has hampered the development of practicable control where Orobanche species are considered to be pests (Grenz et al., 2005; Kusumoto et al., 2007). Indeed, a plethora of physical, cultural, chemical and biological methods have been investigated as potential control approaches against Orobanche, all with limited success, and breeding for resistance is currently perceived to be the most economic, feasible and environmentally friendly method of control (Fernández-Aparicio et al., 2009). Molecular techniques will serve as an important tool for identifying resistance to parasitism; for example, quantitative trait locus (QTL) mapping has greatly promoted the understanding of breeding for resistance in crops attacked by the pernicious parasitic weed Striga (Gurney et al., 2006; Kaewchumnong & Price, 2008;Swarbrick et al., 2008). Control of weedy Orobanche species has been impeded by the emergence of physiological races, in, for example, Orobanche cumana on Helianthus annuus (Bulbul et al., 1991; Fernández-Martínez et al., 2000;Tang et al., 2003), and virulent populations, in, for example, Orobanche crenata on Vicia atropurpurea (Joel, 2000), Phelipanche ramosa (syn. Orobanche ramosa) on Brassica napus, Cannabis sativa and Nicotiana tabacum (Benharrat et al., 2005; Brault et al., 2007), and Orobanche foetida on Cicer arietinum and Vicia faba (Román et al., 2007). These emergent races and populations may evolve under selection pressures stemming from the deployment of individual resistance genes in crop cultivars. Molecular marker-based studies have also demonstrated host–race evolution in the pernicious hemiparasitic weed Striga gesnerioides, (Orobanchaceae) on Indigofera hirsuta and Vigna ungiculata in Central Florida and West Africa (Botanga & Timko, 2005). The process by which physiological races shift from their natural hosts to commercial crops is poorly understood; however, investigations that incorporate data from populations growing on both natural and cultivated hosts will be essential in addressing this knowledge gap (Vaz Patto et al., 2008). We recently demonstrated the potential for host specificity to isolate natural populations of Orobanche and act as a driver for their genetic divergence and speciation (Thorogood et al., 2008, 2009a,b). Our recent data now suggest that compatibility at the cellular level may underpin such patterns of host specificity, and provide a template for host selection and population divergence. In light of the threat to agriculture posed by Orobanche, and the unknown consequences of predicted climate shifts on host range expansion, identifying new host resistance traits to Orobanche is currently crucial. Recently the legume Lotus japonicus was described as an alternative model to Arabidopsis thaliana for studying plant–plant parasitism (Kubo et al., 2009). Similarly, examining resistance pathways using a range of naturally occurring and experimentally tractable host–parasite systems may offer an untapped source of resistance traits that may potentially be integrated into commercial cultivars. Many experiments have cultivated host plants in vitro and artificially infected them with Orobanche to characterize host specificity and mechanisms of resistance, and to identify resistant genotypes of agriculturally important crop species (Rubiales et al., 2004; Pérez-de-Luque et al., 2005a,b; Fernández-Aparicio et al., 2008). Recently, Yoshida & Shirasu (2009) investigated the interactions of Striga hermonthica on various nonhost eudicots, and identified at least four types of incompatibility interaction. The authors suggested that combinations of these different incompatibility interactions may contribute to the total resistance of S. hermonthica. Few studies have investigated host specificity among populations of parasitic plants on their natural hosts. More studies like that of Yoshida & Shirasu (2009) are therefore needed to identify potentially novel sources of resistance mechanisms for commercial crops, using nonhost and natural host species. We examined the compatibility of Orobanche minor and Orobanche picridis on two of their natural hosts, Picris hieracioides and Crepis capillaris, selected on the basis that both species occur naturally on these hosts. Host plants were cultivated in Petri dish bioassays (rhizotrons) in which the infection process could be observed unobtrusively. Host plants were infected reciprocally in four treatments, that is, both host species were infected with both species of parasite. Samples were dissected from bioassays and histological analyses were carried out, following which sections were observed under light microscopy, and under epifluorescence (450–490 nm). Our results revealed distinct incompatibility interactions at developmental checkpoints, reinforcing previous research (Yoder, 1997; Keyes et al., 2001; Yoshida & Shirasu, 2009) and lending weight to the hypothesis that multiple layers of incompatibility may contribute to host specificity in parasitic plants (Yoshida & Shirasu, 2009). Orobanche minor and O. picridis attached to (Fig. 1a), and showed compatible growth on, their natural host associates P. hieracioides and C. capillaris; however, some attachments elicited two distinct resistance responses. The resistance mechanisms observed in this study parallel those described in commercial crop cultivars, suggesting that interactions of Orobanche with their natural hosts are similar at the cellular level. Each of the distinct responses elicited was also indistinguishable among the reciprocal crosses, suggesting that a common mechanism confers resistance to Orobanche attack in these host species. This is consistent with previous studies suggesting that early parasite development is generally nonspecific, and is similar in nonhost as well as host plants (Hood et al., 1998; Yoshida & Shirasu, 2009). Resistance responses in the roots of P. hieracioides and C. capillaris were observed during two main stages in the infection process: an early-acting response when the parasite intrusive cells reached the host root endodermis; and a late-acting response in either tubercles (Fig. 1c,d) or ‘spiders’ (Fig. 1e,f) in which established host–parasite vascular connectivity was obstructed. Together, this indicates that layers of incompatibility contribute to total host specificity in Orobanche, complementing similar evidence recently reported for S. hermonthica (Yoshida & Shirasu, 2009). Incompatibility at the endodermis resulted in the occlusion of vascular tissues by safranin-positive material that obstructed the development of the parasite (Fig. 1b). A similar response has been observed in other systems at various stages of parasite development. For example, secretions were observed in the apoplast at the interface between host and parasite tissues in the roots of vetch (Vicia spp.) in response to infection by Phelipanche aegyptiaca (syn. Orobanche aegyptiaca) (Goldwasser et al., 2000), sunflower roots infected with O. cumana (Labrousse et al., 2001), and carrots infected with P. ramosa (Zehhar et al., 2003). Secretions were also observed in the interaction between O. crenata and its leguminous hosts, where they appeared to cause host xylem occlusion, which, in addition to lignification of endodermal and pericycle host cells, prevented parasite intrusion into the root vascular cylinder at early stages of infection (Pérez-de-Luque et al., 2005b). These secretions appear to originate from parasite cells, and flow through the apoplast to neighbouring host tissues, occluding host vessel elements (Pérez-de-Luque et al., 2005b, 2006). Safranin-staining secretions are probably composed, at least partially, of host cell components released by parasite enzymatic activity (Pérez-de-Luque et al., 2006). Xylem occlusion in incompatibility responses to Orobanche infection have been observed in hosts from taxonomically disparate families, including Fabaceae (Pérez-de-Luque et al., 2005b, 2006), Apiaceae (Zehhar et al., 2003) and Asteraceae (Labrousse et al., 2001). Indeed, occlusion of vascular tissue and lignification are common responses to a range of invading vascular pathogens in plants besides parasitic plants (Beckman, 2000). Our observations of early-acting incompatibility interactions in Orobanche on its natural hosts share similarities with other species in the Orobanchaceae. For example, the haustorium of host generalist hemiparasite Rhinanthus minor on some natural host species becomes encapsulated by lignin, which seals off the host vascular system early in the parasite’s development (Cameron & Seel, 2007). Similarly, S. hermonthica penetrates the host root cortex but does not form vascular connectivity on resistant rice cultivar Nipponbare (Gurney et al., 2006). These similarities in resistance among evolutionarily divergent parasites indicate the widespread importance of early-acting incompatibility interactions in defining host specificity in the Orobanchaceae. Compatible and incompatible interactions of Orobanche at progressive developmental checkpoints contributing to host specificity. (a) Compatible interaction in which the seedling attaches to the host root and produces interfacial parenchyma (IP). (b) Early-acting incompatible interaction in which the parasite is blocked at the endodermis and induces host cortical cell thickening (black arrow) and secretions that block parasite penetration, resulting in tissue death (white arrow), the occlusion of some host xylem vessels (red arrow) and ultimately seedling abortion. (c) Compatible interaction in which the tubercle establishes vascular continuity between parasite (white arrow) and host (black arrow) xylem vessels. (d) Late-acting incompatible interaction in which secretions block xylem vessels with alcian-positive (white arrow) and safranin-positive (black arrow) material, resulting in tubercle abortion. (e) Compatible interaction in which ‘spider’ stage accumulates host-derived starch in amyloplasts (arrow). (f) Late-acting incompatible interaction in which ‘spider’ stage is aborted and parasite xylem vessels are occluded with safranin-positive material (arrow). P, parasite; H, host; E, host root endodermis. Species in photographs: (a, b) Orobanche picridis on Picris hieracioides; (c, d) Orobanche minor on Picris hieracioides; (e, f) O. minor on Crepis capillaris. Further incompatibility at the vascular bundle was characterized by cellular disorganization and a massive occlusion of parasite vascular tissue by both red safranin and green alcian-positive substances (Fig. 1d). Host xylem vessels proximal to the point of infection were also impregnated with safranin-positive material. A similar response has been observed in legume roots infected with O. crenata, in which alcian-positive material appeared to consist of carbohydrates originating in cells neighbouring xylem vessels in host tissues (Pérez-de-Luque et al., 2005b, 2006). These substances may be involved in sealing off endophytic haustorial cells from the host vascular system. Histological studies have also identified parasite cellular disorganization in the sunflower resistance response to O. cumana, which was suggested to be a result of the production of toxic compounds by the host (Labrousse et al., 2001). Together with previous studies, these results suggest that inhibition of parasite development at the endodermis, coupled with excess secretions occluding vascular tissues, may be overarching resistance responses to Orobanche infection in natural hosts and their cultivated counterparts alike. The penetration of root tissues by haustorial cells can be compared with pollen tube growth in stylar tissue (Press et al., 1990), and self-incompatible pollen–pistil interactions are also categorized by early-acting and late-acting mechanisms of pollen tube rejection (Hiscock & Allen, 2008), at least one form of which, characteristic of Papaver (poppy), involves the programmed cell death (PCD) of incompatible pollen tubes (Franklin-Tong & Franklin, 2003; Geitmann et al., 2004;Thomas & Franklin-Tong, 2004). Further work may draw interesting parallels between incompatibility responses in self-incompatibility interactions and host–parasite interactions. Our data, though based on only two host species, consistently identified that a key role in resistance to infection in P. hieracioides and C. capillaris appears to be the endodermis, which acts as a barrier to vascular connectivity, followed by obstruction to host and parasite vascular tissues by the copious secretion of alcian green-positive and safranin-positive staining gel. The resistance mechanisms we characterized are consistent with those described previously in the roots of commercial cultivars, indicating a common pathway of host resistance to parasite infection, and that multiple layers of incompatibility contribute towards host specificity. Future work will screen a range of natural host species to complement investigations using cultivated crops and conventional model species. This study highlights the potential for using natural systems to identify developmental pathways in host–parasite interactions, which may be an important source of novel resistance traits that may be integrated into crop cultivars. The authors thank Alejandro Pérez-de-Luque for his helpful suggestions after critically reading this manuscript. This research was supported by a University of Bristol postgraduate scholarship to C.J.T., along with additional funding from the Lady Emily Smythe Agricultural Research Station (LESARS) of the University of Bristol, and the Botanical Society of the British Isles (BSBI)." @default.
• W2009738587 created "2016-06-24" @default.
• W2009738587 creator A5037843890 @default.
• W2009738587 creator A5074166839 @default.
• W2009738587 date "2010-04-13" @default.
• W2009738587 modified "2023-09-26" @default.
• W2009738587 title "Compatibility interactions at the cellular level provide the basis for host specificity in the parasitic plant <i>Orobanche</i>" @default.
• W2009738587 cites W1486249154 @default.
• W2009738587 cites W1491949502 @default.
• W2009738587 cites W1911808401 @default.
• W2009738587 cites W1944735607 @default.
• W2009738587 cites W1950296352 @default.
• W2009738587 cites W1965504312 @default.
• W2009738587 cites W1969052567 @default.
• W2009738587 cites W1978573387 @default.
• W2009738587 cites W1982440989 @default.
• W2009738587 cites W1990117783 @default.
• W2009738587 cites W1999976787 @default.
• W2009738587 cites W2001177855 @default.
• W2009738587 cites W2011144042 @default.
• W2009738587 cites W2013917806 @default.
• W2009738587 cites W2031265159 @default.
• W2009738587 cites W2032260407 @default.
• W2009738587 cites W2033726288 @default.
• W2009738587 cites W2040462974 @default.
• W2009738587 cites W2041821016 @default.
• W2009738587 cites W2046038960 @default.
• W2009738587 cites W2047902795 @default.
• W2009738587 cites W2048968000 @default.
• W2009738587 cites W2051464866 @default.
• W2009738587 cites W2061123228 @default.
• W2009738587 cites W2069322866 @default.
• W2009738587 cites W2079644601 @default.
• W2009738587 cites W2081319439 @default.
• W2009738587 cites W2094580636 @default.
• W2009738587 cites W2104981392 @default.
• W2009738587 cites W2105227133 @default.
• W2009738587 cites W2105230169 @default.
• W2009738587 cites W2113730786 @default.
• W2009738587 cites W2121594503 @default.
• W2009738587 cites W2125999507 @default.
• W2009738587 cites W2130245085 @default.
• W2009738587 cites W2130524408 @default.
• W2009738587 cites W2135119668 @default.
• W2009738587 cites W2140202694 @default.
• W2009738587 cites W2140401116 @default.
• W2009738587 cites W2144166206 @default.
• W2009738587 cites W2153972841 @default.
• W2009738587 cites W2159063959 @default.
• W2009738587 cites W2160350063 @default.
• W2009738587 cites W2171737635 @default.
• W2009738587 cites W236930874 @default.
• W2009738587 doi "https://doi.org/10.1111/j.1469-8137.2009.03173.x" @default.
• W2009738587 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20522165" @default.
• W2009738587 hasPublicationYear "2010" @default.
• W2009738587 type Work @default.
• W2009738587 sameAs 2009738587 @default.
• W2009738587 citedByCount "20" @default.
• W2009738587 countsByYear W20097385872012 @default.
• W2009738587 countsByYear W20097385872013 @default.
• W2009738587 countsByYear W20097385872014 @default.
• W2009738587 countsByYear W20097385872016 @default.
• W2009738587 countsByYear W20097385872017 @default.
• W2009738587 countsByYear W20097385872018 @default.
• W2009738587 countsByYear W20097385872019 @default.
• W2009738587 countsByYear W20097385872020 @default.
• W2009738587 countsByYear W20097385872021 @default.
• W2009738587 countsByYear W20097385872022 @default.
• W2009738587 countsByYear W20097385872023 @default.
• W2009738587 crossrefType "journal-article" @default.
• W2009738587 hasAuthorship W2009738587A5037843890 @default.
• W2009738587 hasAuthorship W2009738587A5074166839 @default.
• W2009738587 hasConcept C100701293 @default.
• W2009738587 hasConcept C126831891 @default.
• W2009738587 hasConcept C127413603 @default.
• W2009738587 hasConcept C186060115 @default.
• W2009738587 hasConcept C18903297 @default.
• W2009738587 hasConcept C2776033398 @default.
• W2009738587 hasConcept C2776237364 @default.
• W2009738587 hasConcept C2778648169 @default.
• W2009738587 hasConcept C2781200638 @default.
• W2009738587 hasConcept C42360764 @default.
• W2009738587 hasConcept C59822182 @default.
• W2009738587 hasConcept C86803240 @default.
• W2009738587 hasConceptScore W2009738587C100701293 @default.
• W2009738587 hasConceptScore W2009738587C126831891 @default.
• W2009738587 hasConceptScore W2009738587C127413603 @default.
• W2009738587 hasConceptScore W2009738587C186060115 @default.
• W2009738587 hasConceptScore W2009738587C18903297 @default.
• W2009738587 hasConceptScore W2009738587C2776033398 @default.
• W2009738587 hasConceptScore W2009738587C2776237364 @default.
• W2009738587 hasConceptScore W2009738587C2778648169 @default.
• W2009738587 hasConceptScore W2009738587C2781200638 @default.
• W2009738587 hasConceptScore W2009738587C42360764 @default.
• W2009738587 hasConceptScore W2009738587C59822182 @default.
• W2009738587 hasConceptScore W2009738587C86803240 @default.
• W2009738587 hasIssue "3" @default.
• W2009738587 hasLocation W20097385871 @default.

• next