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. 2021 Apr 23;185(4):1292-1308.
doi: 10.1093/plphys/kiaa066.

Adaptation of the parasitic plant lifecycle: germination is controlled by essential host signaling molecules

Affiliations

Adaptation of the parasitic plant lifecycle: germination is controlled by essential host signaling molecules

Harro Bouwmeester et al. Plant Physiol. .

Abstract

Parasitic plants are plants that connect with a haustorium to the vasculature of another, host, plant from which they absorb water, assimilates, and nutrients. Because of this parasitic lifestyle, parasitic plants need to coordinate their lifecycle with that of their host. Parasitic plants have evolved a number of host detection/host response mechanisms of which the germination in response to chemical host signals in one of the major families of parasitic plants, the Orobanchaceae, is a striking example. In this update review, we discuss these germination stimulants. We review the different compound classes that function as germination stimulants, how they are produced, and in which host plants. We discuss why they are reliable signals, how parasitic plants have evolved mechanisms that detect and respond to them, and whether they play a role in host specificity. The advances in the knowledge underlying this signaling relationship between host and parasitic plant have greatly improved our understanding of the evolution of plant parasitism and are facilitating the development of more effective control measures in cases where these parasitic plants have developed into weeds.

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Figures

Figure 1
Figure 1
Lifecycle of root parasitic plants. Seed dormancy release (usually called preconditioning) occurs when exposed to the proper environmental conditions (warm temperature and high moisture). Seed germination occurs upon detection of host germination stimulants by nondormant seeds. Seedlings develop haustoria when exposed to haustorium-inducing factors. The haustorium establishes a connection with the host vasculature, after which a seedling develops that grow belowground for several weeks until emergence. The emerged parasite develops aboveground, flowers, and produces seeds that contribute to the seed bank.
Figure 2
Figure 2
Structures of root parasitic plant germination stimulants.
Figure 3
Figure 3
Schematic representation of strigolactone biosynthesis in a number of different plant species. Bold arrows indicate elucidated enzymatic steps; broken arrows indicated postulated biosynthetic steps. CL, carlactone; CLA, carlactonoic acid; MeCLA, methylcarlactonoate; 5DS, 5-deoxystrigol; 4DO, 4-deoxyorobanchol.
Figure 4
Figure 4
Schematic representation of the perception of germination stimulants through the HTL receptors and the effect of differences in affinity. Germination stimulants (GS1 and 2) bind to an HTL that then recruits MAX2. The activated complex degrades downstream repressor, SMAX, which results in de-repression of gene expression and induces germination. In case of low affinity of the HTL present in the seed for the host germination stimulant, signal transduction and germination do not occur. Host-specific germination in root parasitic plants could be driven by affinity differences between HTLs for host-produced germination stimulants.

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