Valentine Otang Ntui, Edak Aniedi Uyoh, Effiom Eyo Ita, Aniedi-Abasi Akpan Markson, Jaindra Nath Tripathi, Nkese Ime Okon, Mfon Okon Akpan, Julius Oyohosuho Phillip, Ebiamadon Andi Brisibe, Ene-Obong Effiom Ene-Obong, Leena Tripathi

Molecular Plant Biology; Published on line 17 July 2021. https://doi.org/10.1111/mpp.13107

Abstract

Yam (Dioscorea spp.) anthracnose, caused by Colletotrichum alatae, is the most devastating fungal disease of yam in West Africa, leading to 50%–90% of tuber yield losses in severe cases. In some instances, plants die without producing any tubers or each shoot may produce several small tubers before it dies if the disease strikes early. C. alatae affects all parts of the yam plant at all stages of development, including leaves, stems, tubers, and seeds of yams, and it is highly prevalent in the yam belt region and other yam-producing countries in the world. Traditional methods adopted by farmers to control the disease have not been very successful. Fungicides have also failed to provide long-lasting control. Although conventional breeding and genomics-assisted breeding have been used to develop some level of resistance to anthracnose in Dioscorea alata, the appearance of new and more virulent strains makes the development of improved varieties with broad-spectrum and durable resistance critical. These shortcomings, coupled with interspecific incompatibility, dioecy, polyploidy, poor flowering, and the long breeding cycle of the crop, have prompted researchers to explore biotechnological techniques to complement conventional breeding to speed up crop improvement. Modern biotechnological tools have the potential of producing fungus-resistant cultivars, thereby bypassing the natural bottlenecks of traditional breeding. This article reviews the existing biotechnological strategies and proposes several approaches that could be adopted to develop anthracnose-resistant yam varieties for improved food security in West Africa.

See: https://bsppjournals.onlinelibrary.wiley.com/doi/10.1111/mpp.13107

Figure 2; Schematic representation of the CRISPR/Cas9 gene editing mechanism. gRNA directs Cas9 to cleave the target sequence upstream of the protospacer adjacent motif (PAM), producing a double-stranded break (DSB). The DSB is subsequently repaired either by nonhomologous end-joining (NHEJ) or by homology-directed repair (HDR). Repair via NHEJ produces indels (knockout), whereas repair through HDR results in knockin.