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Cassava is a major staple, bio-energy and industrial crop in many parts of the developing world. In Southeast Asia, cassava is grown on >4 million ha by nearly 8 million (small-scale) farming households, under (climatic, biophysical) conditions that often prove unsuitable for many other crops. While SE Asian cassava has been virtually free of phytosanitary constraints for most of its history, a complex of invasive arthropod pests and plant diseases has recently come to affect local crops. We describe results from a region-wide monitoring effort in the 2014 dry season, covering 429 fields across five countries. We present geographic distribution and field-level incidence of the most prominent pest and disease invaders, introduce readily-available management options and research needs. Monitoring work reveals that several exotic mealybug and (red) mite species have effectively colonised SE Asia's main cassava-growing areas, occurring in respectively 70% and 54% of fields, at average field-level incidence of 27 ± 2% and 16 ± 2%. Cassava witches broom (CWB), a systemic phytoplasma disease, was reported from 64% of plots, at incidence levels of 32 ± 2%. Although all main pests and diseases are non-natives, we hypothesise that accelerating intensification of cropping systems, increased climate change and variability, and deficient crop husbandry are aggravating both organism activity and crop susceptibility. Future efforts need to consolidate local capacity to tackle current (and future) pest invaders, boost detection capacity, devise locally-appropriate integrated pest management (IPM) tactics, and transfer key concepts and technologies to SE Asia's cassava growers. Urgent action is needed to mobilise regional as well as international scientific support, to effectively tackle this phytosanitary emergency and thus safeguard the sustainability and profitability of one of Asia's key agricultural commodities. © 2016 Society of Chemical Industry.

Victorin, the host-selective toxin produced by the fungus Cochliobolus victoriae, induces programmed cell death (PCD) in victorin-sensitive oat lines with characteristic features of animal apoptosis, such as mitochondrial permeability transition, chromatin condensation, nuclear DNA laddering and rRNA/mRNA degradation. In this study, we characterized a calcium-binding protein, namely AsALG-2, which might have a role in the victorin-induced PCD. AsALG-2 is homologous to the Apoptosis-Linked Gene ALG-2 identified in mammalian cells. Northern blot analysis revealed that the accumulation of AsALG-2 transcripts increased during victorin-induced PCD, but not during necrotic cell death. Salicylic acid, chitosan and chitin strongly activated the expression of general defence response genes, such as PR-10; however, neither induced cell death nor the accumulation of AsALG-2 mRNA. Pharmacological studies indicated that victorin-induced DNA laddering and AsALG-2 expression were regulated through similar pathways. The calcium channel blocker, nifedipine, moderately inhibited the accumulation of AsALG-2 mRNA during cell death. Trifluoperazine (calmodulin antagonist) and K252a (serine-threonine kinase inhibitor) reduced the victorin-induced phytoalexin accumulation, but did not prevent the victorin-induced DNA laddering or accumulation of AsALG-2 mRNA. Taken together, our investigations suggest that there is a calcium-mediated signalling pathway in animal and plant PCD in common.

Here we report that rRNA and mRNA are specifically degraded in oat (Avena sativa L.) cells during apoptotic cell death induced by victorin, a host-selective toxin produced by Cochliobolus victoriae. Northern analysis indicated that rRNA species from the cytosol, mitochondria and chloroplasts were all degraded via specific degradation intermediates during victorin-induced apoptotic cell death but, in contrast, they were randomly digested in necrotic cell death induced by 30 mM CuSO(4) and heat shock. This indicates that specific rRNA cleavage could be controlled by an intrinsic program. We also observed specific cleavage of mRNA of housekeeping genes such as actin and ubiquitin during victorin-induced cell death. Interestingly, no victorin-induced mRNA degradation was detected with stress-responding genes such as PR-1, PR-10 and GPx throughout the experimental period. The RNA degradation mostly, but not always, occurred in parallel with DNA laddering, but pharmacological studies indicated that these processes are regulated by different signaling pathways with some overlapping upstream signals.