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Habits of a highly successful cereal killer, Striga

Habits of a highly successful cereal killer, Striga

  • Steven Runo, 
  • Eric K. Kuria


Striga is a highly successful pathogen of cereal crops in sub-Saharan Africa. Also known as witchweed, Striga is an attractive parasitic plant whose beautiful flowers belie its noxiousness. Most cultivated cereals, including maize, millet, sorghum, and rice, are parasitized by at least one Striga species, leading to enormous economic losses. Control strategies are limited but include common agronomic practices of hand weeding, crop rotation, and general sanitization techniques. Striga-resistant crops, as well as tolerant ones, have also been used, but this resistance tends to break down with the emergence of new Striga variants. With limited and ineffective management options, Striga has continued to increase both its host range and area under infestation. In this article, we outline seven unique characteristics of Striga as a parasite of great economic importance, explore reasons for its success, and outline emerging control options.

1. Diversity

The Striga genus has many species that are widely distributed, each with different host preferences. While some Striga species can only infect one or a few host species, others can infect many host genera. The diversity in host preference by members of the Striga genus ensures ease of finding suitable hosts, which helps expand its range. Consequently, Striga has been able to expand from its native range in the Semien hills of Ethiopia and the Nubian Hills of Sudan to over 40 countries in Africa [1]. In infested fields, Striga causes 20% to 100% crop losses as illustrated in Fig 1A. Such crop losses lead to great economic losses. For example, Striga causes an estimated loss of $111 million to $200 million annually in rice alone [2].

Fig 1. Witchweed (Striga) at a glance.

(a) Destructive effect of S. hermonthica at high infestation (right), where Striga has caused complete crop failure, compared with low infestation (left), where some yields can be realized. Other effects of Striga infestation such as chlorosis can be observed on the field in the right (red arrows). This picture was taken in a farmer’s maize field in Gem, Siaya County in Western Kenya. Photo credit Daniel Ajaku (ICRISAT). (b) Striga small seeds in comparison with sorghum. The tiny dust-like seeds can remain dormant in soil for decades. Scale bar = 5 mm. (c) Striga seedlings 12 hours after treating with a germination stimulant (GR24). Striga seeds germinate only in response to chemical cues from the host plant. Scale bar = 0.5 mm. (d) A 10-day–old Striga seedling with a well-developed haustorium attached to a sorghum root. Scale bar = 0.2 mm. (e) A schematic of a section through a 10-day–old Striga seedling showing the parasite (P) attached to a host (H). By this time, the parasite has developed fully. The parasite xylem (Px) has merged with the host xylem (Hx) to form a siphon (Hx-Px) that sucks out nutrients from the host. Scale bar = 0.05 mm. H, host; Hx, host xylem; ICRISAT, International Crops Research Institute for the Semi-Arid Tropics; P, parasite; Px, parasite xylem.

With regard to specific species distribution and host range, S. hermonthica’s range extends throughout Eastern Africa in Kenya, Uganda, Tanzania, Ethiopia, Sudan, Rwanda, and Burundi as well as in West Africa, where it parasitizes maize, millet, sorghum, and upland rice. S. asiatica occurs in both Southern and Eastern Africa, the Arabian Peninsula, India, and Pakistan and is parasitic to rice, sorghum, and millet. S. gesnerioides infects dicotyledonous plants, greatly limiting cowpea production in the West African countries of Mali, Burkina Faso, Niger, and Benin. Finally, S. aspera constrains maize and rice production in Sudan, Malawi, Nigeria, Cameroon, Ivory Coast, and Senegal [3].

2. Fecundity

Fruitfulness and fertility in biology are used to describe an organism that is able to produce a large number of viable offspring. A single Striga plant produces 50,000 to 500,000 seeds [4]. Such high fecundity provides Striga with high epidemiological potential because of the exponential increase in pathogen population from one generation to the next.

3. Mobility

Striga seeds are small (about 0.2 mm in length) and dust-like (Fig 1B). Striga’s small seed size greatly enhances the parasite’s dispersal by wind, water, and contaminated crop seeds. The small-sized seeds also adhere to people and animals, further aiding in seed spread and contamination of uninfected fields. However, a small Striga seed size means that the endosperm can only support growth for three to seven days [4]. Therefore, germination must be rapid and synchronized with host localization.

4. Coordinated

The Striga parasitic life cycle is highly synchronized with its host and involves the following three general phases: germination, haustorium formation, and penetration (Fig 1C, 1D and 1E). Germination only occurs in the presence of a suitable host, which Striga locates using plant hormones called strigolactones. Physiologically, strigolactones function to inhibit shoot branching in plants [5] but also serve as cues for colonization by phosphate (P)-mobilizing symbionts such as arbuscular mycorrhiza fungi (AMF) [6]. Accordingly, when P levels in soil fall, plant roots exude strigolactone to increase mycorrhization by AMF. However, Striga “eavesdrops” on this conversation and hijacks the signal [6]. Strigolactone then binds to receptors—KARRAKIN-INSENSITIVE 2 (KAI2)/HYPERSENSITIVE TO LIGHT (HTL) [7]—in Striga seeds, causing the receptor to recruit an F-box protein that degrades germination-inhibiting transcriptional regulators. These series of events trigger Striga seed germination [8].

Following germination, the Striga radicle attaches to the host and differentiates into a specialized organ—the haustorium (Fig 1D and 1E) [9]. Like in germination, the haustorium develops in response to chemical cues from the host, the haustorial inducing factors such as 2,6-dimethoxy-p-benzoquinone (DMBQ) [10].

Finally, the haustorium penetrates the host until it encounters the endodermis, where haustorial cells elongate and divide to establish vascular connections with the host (Fig 1D and 1E). Once the vascular systems of the host and parasite are connected, Striga uses this connection to siphon out nutrients.

5. Dormancy

In the absence of the germination signal, Striga exhibit high dormancy and longevity. Striga seeds can remain dormant in soil for up to 10 years, waiting for the appropriate host to attack [11]. The parasite’s ability to “cool off” for extended periods of time is important in its life cycle because it renders the parasite resistant to herbicides as well as decay-inducing organisms.

6. Manipulative

Striga reprograms the host in ways that are beneficial to its parasitism. It has been shown that (i) Striga is able to alter levels of important hormone such as abscisic acid (ABA), cytokinins, and gibberellic acid during infection [12] and (ii) acquire genes from its host and modify them for parasite use [13].

Furthermore, it is now emerging that Striga is a sophisticated manipulator of host immunity [14]. Plausibly, Striga is able to subdue host defense by producing a battery of molecules (effectors), just like bacterial and fungal pathogens. Although identification and characterization of effector genes from Striga has not been carried out, race-specific activation of host defense response lends credence to this hypothesis. It has been shown that in a S. gesnerioides–resistant cowpea variety (b301), hypersensitive reaction (HR) immunity is only activated by the hypervirulent S. gesnerioides race 3 (SG3) from Nigeria and Niger [15].

The Striga effector paradigm is more plausible when one draws extrapolations from other parasitic plant–host interactions. For example, potential effectors have been recently described in Orobanche ramosaArabidopsis [16] and in the Cuscuta reflexa–tomato interactions [17].

7. Mysterious

Striga’s common name, “witchweed,” is derived from the mysterious drought-like symptoms, wilting, and chlorosis seen in Striga-infected plants even before the parasite emerges from soil (Fig 1A). This effect occurs very soon after infection—as early as one week after infection—and cannot be attributed to simply Striga sucking out nutrients from the host. It has been long suggested that Striga injects yet-to-be-identified phytotoxins to its hosts during parasitism, causing the “bewitching” phenotype [18]. Although research on detailed characterization of the toxin and its mechanisms of action remains elusive, support for the hypothesis that Striga contains powerful secondary metabolites that help the parasite subdue its hosts can be derived from phytochemical studies of Striga extracts, for example iridoid glucosides [19]. Although not toxic themselves, iridoic glycosides are easily converted to toxic aglycone moiety [20], which poisons cells by denaturing proteins.

Summary and perspectives

Characteristics of Striga described above are indicative of a successful pathogen whose control should take into account biological and chemical mechanisms underpinning Striga–host interaction. Therefore, common emerging Striga control strategies are aimed at (i) exploiting host-based resistance, (ii) evading Striga germination, and (iii) depleting the vast Striga seedbank in soil.

Exploiting host-based resistance

Some crops and their wild relatives are able to block Striga penetration through biochemical [21] or mechanical [22] barriers. In addition, some Striga hosts resist parasitism by triggering an HR at the site of infection [15]. Current advances in genomics and molecular genetics provide tools for “pinpointing” resistance genes and/or loci through genome-wide association mapping and transcriptome profiling. Identified genes and/or loci can then be combined (pyramided) to provide durable resistance.

Evading Striga germination

Some crop varieties produce variants of strigolactone that do no induce Striga germination effectively. In sorghum, this was found to be due to a mutation on the LOW GERMINATION STIMULANT 1 (LGS1) locus [23]. This development provides prospects for manipulating the strigolactone production pathway in crops—using genome-editing tools—in order to develop crop varieties less potent in inducing Striga germination. Striga germination can also be blocked by small molecules that bind to the strigolactone receptor in Striga as antagonist [24], pointing to the possibility of using chemical biology technology in Striga control.

Depleting Striga seedbank

Chemical molecules that mimic the activity of strigolactones present a new frontier in Striga control because such molecules can cause the parasite to germinate in the absence of a host—a strategy known as suicidal germination [25]. This technology was previously not feasible due to the high cost associated with multistep chemical synthesis of strigolactones as well as their instability under field conditions. It is now possible to synthesize simple strigolactone analogues that, when treated with chemical formulations, retain activity and stability under field conditions [25]. This approach is attractive because in the short term, it can lead to a significant reduction of Striga seeds in soil.

In summary, while advances in science provide additional tools for Striga control, these measures should be employed in combination with more traditional approaches such as crop rotation and sanitizing to minimize Striga seed increase and spread to noncontaminated fields.


  1. 1. Ejeta G. The Striga scourge in Africa: A growing pandemic. In: Gressel J, editor. Integrating new technologies for Striga control: Towards ending the witch-hunt. 1 st. London: World Scientific Publishing co. pte. Ltd; 2007. pp. 3–15.
  2. 2. Rodenburg J, Demont M, Zwart SJ, Bastiaans L. Parasitic weed incidence and related economic losses in rice in Africa. Agric Ecosyst Environ. Elsevier B.V.; 2016;235: 306–317.
  3. 3. Parker C. Parasitic weeds: A world challenge. Weed Sci. 2012;60: 269–276.
  4. 4. Berner DK, Kling JG, Singh BB. Striga research and control: A perspective from Africa. Plant Dis. 1995;79: 652–660.
  5. 5. Umehara M, Hanada A, Yoshida S, Akiyama K, Arite T, Takeda-Kamiya N, et al. Inhibition of shoot branching by new terpenoid plant hormones. Nature. 2008;455: 195–200. pmid:18690207
  6. 6. Bouwmeester HJ, Roux C, Lopez-Raez JA, Bécard G. Rhizosphere communication of plants, parasitic plants and AM fungi. Trends Plant Sci. 2007;12: 224–30. pmid:17416544
  7. 7. Toh S, Holbrook-Smith D, Stogios PJ, Onopriyenko O, Lumba S, Tsuchiya Y, et al. Structure-function analysis identifies highly sensitive strigolactone receptors in Striga. Science. 2015;350: 203–7. pmid:26450211
  8. 8. Lumba S, Holbrook-smith D, Mccourt P. The perception of strigolactones in vascular plants. Nat Chem Biol. 2017;13: 599–606. pmid:28514432
  9. 9. Dörr I. How Striga parasitizes its Host: a TEM and SEM study. Ann Bot. 1997;79: 463–472.
  10. 10. Estabrook EM, Yoder JI. Update on plant-plant communication: Rhizosphere signaling between parasitic angiosperms and their hosts. Plant Physiol. 1998;116: 1–7.
  11. 11. Atera E, Itoh K. Evaluation of ecologies and severity of Striga weed on rice in sub-Saharan Africa. Agric Biol J North Am. 2011;2: 752–760.
  12. 12. Frost DL, Gurney AL, Press MC, Scholes JD. Striga hermonthica reduces photosynthesis in sorghum: the importance of stomatal limitations and a potential role for ABA? Plant, Cell Environ. 1997;20: 483–492.
  13. 13. Yang Z, Wafula EK, Honaas LA, Zhang H, Das M, Fernandez-aparicio M, et al. Comparative transcriptome analyses reveal core parasitism genes and suggest gene duplication and repurposing as sources of structural novelty. Mol Biol Evol. 2014;32: 767–790. pmid:25534030
  14. 14. Saucet SB, Shirasu K. Molecular parasitic plant–host interactions. PLoS Pathog. 2016;12: 1–6. pmid:27977782
  15. 15. Li J, Timko MP. Gene-for-gene resistance in Striga -cowpea associations. Science (80-). 2009;325: 1094. pmid:19713520
  16. 16. El-Maarouf-Bouteau H, Moreau E, Errakhi R, Sallé G. A diffusible signal from germinating Orobanche ramosa elicits early defense responses in suspension-cultured Arabidopsis thaliana. Plant Signal Behav. 2008;3: 189–193. pmid:19513214
  17. 17. Hegenauer V, Fürst U, Kaiser B, Smoker M, Zipfel C. Detection of the plant parasite Cuscuta reflexa by a tomato cell surface receptor. Science. 2016;353: 478–481. pmid:27471302
  18. 18. Musselman LJ. The biology of Striga, Orobanche, and other root-parasitic weeds. Annu Rev Phytopathol. Annual Reviews; 1980;18: 463–489.
  19. 19. Rank C, Rasmussen LS, Jensen SR, Pierce S, Press MC, Scholes JD. Cytotoxic constituents of Alectra and Striga species. Weed Res. 2004;44: 265–270.
  20. 20. Konno K, Hirayama C, Yasui H, Nakamura M. Enzymatic activation of oleuropein: A protein crosslinker used as a chemical defense in the privet tree. Proc Natl Acad Sci. 1999;96: 9159–9164. pmid:10430912
  21. 21. Mbuvi DA, Masiga CW, Kuria EK, Masanga J, Wamalwa M, Mohamed A, et al. Novel sources of witchweed (Striga) resistance from wild sorghum accessions. Front Plant Sci. 2017;8: 1–15.
  22. 22. Gurney AL, Slate J, Press MC, Scholes JD. A novel form of resistance in rice to the angiosperm parasite Striga hermonthica. New Phytol. 2006;169: 199–208. pmid:16390431
  23. 23. Gobena D, Shimels M, Rich PJ, Ruyter-spira C, Bouwmeester H, Kanuganti S. Mutation in sorghum LOW GERMINATION STIMULANT 1 alters strigolactones and causes Striga resistance. Proc Natl Acad Sci. 2017;114: 4471–4476. pmid:28396420
  24. 24. Holbrook-Smith D, Toh S, Tsuchiya Y, McCourt P. Small-molecule antagonists of germination of the parasitic plant Striga hermonthica. Nat Chem Biol. Nature Publishing Group; 2016;12: 724–729. pmid:27428512
  25. 25. Zwanenburg B, Pospisil T, Zeljkovic S. Strigolactones: new plant hormones in action. Planta. 2016;243: 1311–1326. pmid:26838034