The genetic basis of plants' battle against witchweeds: linking immune responses to distinct resistance mechanisms

Abstract

This article comments on:

Mutinda S, Mobegi FM, Hale B, Dayou O, Ateka E, Wijeratne A, Wicke S, Bellis ES, Runo S. 2023. Resolving intergenotypic Striga resistance in sorghum. Journal of Experimental Botany 74, 5294–5306.

Keywords: Striga; Cell type-specific defence; cell wall-based resistance; hypersensitive response; inducible defence; lignin; parasitic plants; post-attachment resistance.

Fig. 1.

Host resistance responses during different stages of the Striga life cycle. (A) Pre-attachment resistance response during Striga seed germination. Host plants growing in nutrient-poor soil release strigolactones, promoting beneficial arbuscular mycorrhizal fungus symbiosis. Striga seeds perceive these host strigolactones as germination stimulants. However, mutations in genes responsible for strigolactone biosynthesis or alterations in their composition significantly reduce Striga seed germination rates. For example, mutations in the LOW GERMINATION STIMULANT 1 (LGS1) gene in resistant sorghum plants alter the composition of strigolactones in root exudates, reducing their stimulatory effect on Striga germination. (B) Pre-attachment resistance response during haustorium initiation. Germinated Striga seedlings grow towards host roots and perceive haustorium induction factors (HIFs) for haustorium initiation. Resistant host plants produce toxic compounds in root exudates that inhibit the development of parasitic plant seedlings (Box 1). Some resistant host plants produce lower levels of HIFs, reducing Striga haustorium formation (Box 1). (C) Post-attachment resistance response during haustorium attachment. Following the detection of pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) from Striga, plants initiate pattern-triggered immunity (PTI) to obstruct haustorium attachment. However, parasitic plant effectors can suppress PTI to facilitate parasitism. Consequently, effector-triggered immunity (ETI) overcomes this suppression and triggers hypersensitive responses (HRs) to discourage parasite penetration. (D) Post-attachment resistance response during haustorium vascular connection. Plants fortify cell walls to create physical barriers that hinder the establishment of vascular connections. According to the study by Mutinda et al., cell wall enhancement-based resistance responses probably occur downstream of PTI and ETI. Examples of these barriers include accumulating substances such as lignin or callose in the cortex, impeding the progress of parasites. Moreover, the endodermis serves as a barrier by inducing lignin accumulation, effectively preventing parasitic plant penetration and vascular connection. More details are described in Fig. 2. Three-dimensional structure images of orobanchol (Compound CID: 10665247), 5-deoxystrigol (Compound CID: 15102684), lignin (Compound CID: 175586), and callose (beta-d-glucose, Compound CID: 64689) are exported from PubChem. This figure was created with https://www.biorender.com/.

Fig. 2.

Cell type-specific barriers and defence mechanisms safeguarding host plants against root-parasitic plant invasion. Plant cell type-specific barriers and defence mechanisms play a vital role in protecting plants against root-parasitic plant invasion. Notable examples of these protective barriers include: (A) concentrated accumulation of phenolic compounds in the epidermis and endodermis, (B) localized deposition of lignin in the cortex and endodermis, (C) targeted accumulation of silica in the endodermis, and (D) confined build up of callose in the cortex. Three-dimensional structure images of phenolic compounds (4-hydroxycinnamic-acid, Compound CID: 637542), lignin (Compound CID: 175586), silica (silicon dioxide, Compound CID: 24261) and callose (beta-d-glucose, Compound CID: 64689) are exported from PubChem. This figure is created with https://www.biorender.com/.