Wood vinegar (WV) is a biostimulant and a biopesticide that contains pyroligneous acid and is used as a crop growth enhancer and biocontrol agent, but insufficient information exists on WV’s effects on soil quality and cowpea production in Ghana. A field study (2 years) was conducted to determine the appropriate method of applying WV for soil health and cowpea production, and to determine the economic benefits of WV. Assessments were on nodulation, shoot biomass, yield, value–cost ratio, soil enzymes, soil respiration, microbial biomass nitrogen (MBN), permanganate-oxidizable carbon (POXC), mineralizable C, soil pH, available nitrogen and phosphorus. Results revealed soil drenching and foliar application are efficient methods of applying WV to achieve greater shoot dry matter, nodulation and grain yield of cowpea. Economically, soil drenching, followed by foliar application, generated better economic returns than the control. Adding WV to cowpea using soil drenching and foliar application improved soil health indicators. Soil enzymes and MBN were enhanced by WV applied foliarly and through soil drenching. Soil drenching with WV produced greater POXC and mineralizable C compared to the other treatments. Conclusively, WV applied foliarly and through soil drenching improved soil health, nodulation and yields of cowpea, and enhanced profitability.

Toxic metabolites known as aflatoxins are produced via certain species of the Aspergillus genus, specifically A. flavus, A. parasiticus, A. nomius, and A. tamarie. Although various pre- and post-harvest strategies have been employed, aflatoxin contamination remains a major problem within peanut crop, especially in subtropical environments. Aflatoxins are the most well-known and researched mycotoxins produced within the Aspergillus genus (namely Aspergillus flavus) and are classified as group 1 carcinogens. Their effects and etiology have been extensively researched and aflatoxins are commonly linked to growth defects and liver diseases in humans and livestock. Despite the known importance of seed coats in plant defense against pathogens, peanut seed coat mediated defenses against Aspergillus flavus resistance, have not received considerable attention. The peanut seed coat (testa) is primarily composed of a complex cell wall matrix consisting of cellulose, lignin, hemicellulose, phenolic compounds, and structural proteins. Due to cell wall desiccation during seed coat maturation, postharvest A. flavus infection occurs without the pathogen encountering any active genetic resistance from the live cell(s) and the testa acts as a physical and biochemical barrier only against infection. The structure of peanut seed coat cell walls and the presence of polyphenolic compounds have been reported to inhibit the growth of A. flavus and aflatoxin contamination; however, there is no comprehensive information available on peanut seed coat mediated resistance. We have recently reviewed various plant breeding, genomic, and molecular mechanisms, and management practices for reducing A. flavus infection and aflatoxin contamination. Further, we have also proved that seed coat acts as a physical and biochemical barrier against A. flavus infection. The current review focuses specifically on the peanut seed coat cell wall-mediated disease resistance, which will enable researchers to understand the mechanism and design efficient strategies for seed coat cell wall-mediated resistance against A. flavus infection and aflatoxin contamination.

Aflatoxin contamination is a global menace that adversely affects food crops and human health. Peanut seed coat is the outer layer protecting the cotyledon both at pre- and post-harvest stages from biotic and abiotic stresses. The aim of the present study is to investigate the role of seed coat against A. flavus infection. In-vitro seed colonization (IVSC) with and without seed coat showed that the seed coat acts as a physical barrier, and the developmental series of peanut seed coat showed the formation of a robust multilayered protective seed coat. Radial growth bioassay revealed that both insoluble and soluble seed coat extracts from 55-437 line (resistant) showed higher A. flavus inhibition compared to TMV-2 line (susceptible). Further analysis of seed coat biochemicals showed that hydroxycinnamic and hydroxybenzoic acid derivatives are the predominant phenolic compounds, and addition of these compounds to the media inhibited A. flavus growth. Gene expression analysis showed that genes involved in lignin monomer, proanthocyanidin, and flavonoid biosynthesis are highly abundant in 55-437 compared to TMV-2 seed coats. Overall, the present study showed that the seed coat acts as a physical and biochemical barrier against A. flavus infection and its potential use in mitigating the aflatoxin contamination.

Aflatoxins, which have been classified as a group-1 carcinogen are the well-known mycotoxins produced by Aspergillus flavus. Aflatoxins have been linked to liver diseases, acute hepatic necrosis, resulting in cirrhosis or hepatocellular carcinomas due to which it incurs a loss of value in international trade for peanuts contaminated with it. The four main aflatoxins are B1, B2, G1, and G2 of which B1 is predominant. In plants, the cell wall is the primary barrier against pathogen invasion. Cell wall fortifications such as deposition of callose, cellulose, lignin, phenolic compounds and structural proteins help to prevent the pathogen infection. Further, the host cell’s ability to rapidly repair and reinforce its cell walls will result in a reduction of the penetration efficiency of the pathogen. Peanut seed coat acts as a physical and biochemical cell wall barrier against both pre and post-harvest pathogen infection. The structure of seed coat and the presence of polyphenol compounds have been reported to inhibit the growth of A. flavus, however, not successfully employed to develop A. flavus resistance in peanut. A comprehensive understanding of peanut seed coat development and biochemistry will provide information to design efficient strategies for the seed coat mediated A. flavus resistance and Aflatoxin contamination.