New pre-attachment Striga resistant sorghum adapted to African agro-ecologies

asiatica occurs in sorghum mutants designated low germination stimulant 1 (lgs1). However, only a few of these mutants have been identified and their resistance validated. The Striga lifecycle, which is closely synchronized with the life-cycles of its hosts, contributes to its success. Striga has microscopic seeds that disperse easily, stay dormant in soil for decades, and germinate only in response to host-derived signaling molecules. These signaling molecules, now known to be a class of novel plant hormones that regulate root and shoot architecture, are exuded in the roots of host and many non-host species, and act as seed germination stimulants. The tightly regulated germination stage in the Striga lifecycle provides opportunities for parasite control prior to attachment to the host. These mechanisms, generally termed pre-attachment resistance, are caused by production of Striga growth inhibitors (allelopathy), less-efficient Striga seed germination stimulation, or poor haustorium formation. Sorghum itself is known to have many plant growth-inhibiting compounds such as dhurrin, phenolic acids, and sorgoleone, although none has been tested and found to have allelopathic activity against Striga. Striga resistance is known to occur in the East African sorghum breeding line SRN39 based on low germination induction. The root exudate of this genotype is composed mainly of a strigolactone called orobanchol that does not effectively stimulate germination of Striga, contrary to susceptible genotypes that produce the highly active germination stimulant 5-deoxystrigol. A mutation in the lgs1 locus leads to functional loss of a sulfotransferase gene and is designated lgs1-1. The lgs1 locus is much larger and comprises a cluster of genes that extend from position 69 977 147 to position 70 011 172 on chromosome 5 of sorghum, where other lgs1 mutations that also cause low germination activity have been identified and designated lgs1-2, lgs1-3, lgs1-4, and lgs1-5. Based on a report by Bells et al. showing evolutionary adaptation of sorghum to Striga parasitism, it was hypothesized that lgs1 is widespread in sub-Saharan Africa. To test these hypotheses, a subset of the Generation Challenge Program sorghum reference set (RS) was screened for pre-attachment resistance using germination assays that determined germination and radicle size of Striga seedlings, and lgs1-like mutations using microsatellite markers previously described by Satish et al. and a sulfotransferase specific marker described by Gobena et al. Seeds of 177 sorghum accessions from the reference set were obtained from ICRISAT, Nairobi, Kenya, and SRN39 and IS9830, both originally from Sudan, and known to harbor the lgs1 mutation, were used as resistant controls; the Kenyan landrace Ochuti was used as a susceptible control. Seeds of S. hermonthica were collected in 2016 from Kibos near Kisumu (0.0699°S, 34.8169°E) in western Kenya and maintained at the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT, Patancheru, India). The sorghum collection was evaluated for pre-attachment resistance against Striga using an in vitro assay that measured Striga germination activity and radicle growth. From a total of 177 sorghum accessions, 60 recorded mean germination levels of below 42%, which is comparable with the previously identified lgs1-like sorghum (SRN39 and IS9830) used as controls in this study. Furthermore, 32 of these accessions recorded Striga radicle lengths comparable or lower than the controls (0.42 mm). Thirty-eight accessions contained the lgs1 mutation, and although overall, lgs1 mutants had considerably reduced Striga germination, some low inducers of Striga germination were wild-type for lgs1. Germination was positively but weakly correlated with radicle length, pointing to additional radicle growth inhibitory activity.