bioRxiv Science⌕ Search

Biology subjects

Oppong, A.

Publications and source records attributed to Oppong, A..

2 recordsLinked to original sources

Predicting the cross-continental spread of the cassava brown streak disease epidemic in sub-Saharan Africa

Cassava brown streak disease (CBSD) is a major threat to smallholder farmers in sub-Saharan Africa (SSA), where cassava is a staple crop. Caused by cassava brown streak ipomoviruses (CBSIs), CBSD has spread extensively since its detection in Uganda in 2004, raising concerns about ongoing spread through Southern and Central Africa and potential expansion to West Africa, home to the worlds largest cassava producer, Nigeria. Building on a stochastic epidemiological model that predicts CBSD spread at the scale of Uganda, we incorporate extensive field surveillance records to extend the model to all thirty-two major cassava-producing countries in SSA. We then deploy the model to address key strategic questions such as estimating the present day CBSD distribution and predicting rates of ongoing spread towards West Africa. We also evaluate the risk of direct introductions resulting from long range movement of infected planting material, which could trigger outbreaks beyond predicted localised dispersal limits. Our model predicts the likely arrival of CBSD in Nigeria via cross-continental spread within 25 years, and if directly introduced anywhere in West Africa, spreading to most West African nations within 10 years. The risks of ongoing and future CBSD spread highlighted in this study underscore the need for proactive phytosanitation measures, including clean seed programs, vector control, and quarantine policies to curb CBSD spread. Moreover, the model described in this study not only provides estimates for arrival times across SSA, but also lays the foundations for a continental-scale quantitative framework wherein both surveillance and management options can be explored and optimised.

ecology↗

14-3-3ζ regulates lipolysis by influencing adipocyte maturity

One of the primary metabolic functions of a mature adipocyte is to supply energy via lipolysis, or the catabolism of stored lipids. Hormone-sensitive lipase (HSL) is a critical lipolytic enzyme, and its phosphorylation and subsequent activation by PKA generates phospho-binding sites for 14-3-3 proteins, a ubiquitously expressed family of molecular scaffolds. While we previously identified essential roles of the 14-3-3{zeta} isoform in murine adipogenesis, the presence of 14-3-3 protein binding sites on HSL suggests that 14-3-3{zeta} could also influence mature adipocyte processes like lipolysis. Herein, we demonstrate that 14-3-3{zeta} is necessary for lipolysis in male mice and fully differentiated 3T3-L1 adipocytes, as depletion of 14-3-3{zeta} significantly impaired glycerol and FFA release. Unexpectedly, this was not due to impairments in signaling events underlying lipolysis; instead, reducing 14-3-3{zeta} expression was found to significantly impact adipocyte maturity, as observed by reduced abundance of PPAR{gamma}2 protein and expression of mature adipocytes genes and those associated with de novo triglyceride synthesis and lipolysis. The impact of 14-3-3{zeta} depletion on adipocyte maturity was further examined with untargeted lipidomics, which revealed that reductions in 14-3-3{zeta} abundance promoted the acquisition of a lipidomic signature that resembled undifferentiated, pre-adipocytes. Collectively, these findings reveal a novel aspect of 14-3-3{zeta} in adipocytes, as reducing 14-3-3{zeta} was found to have a negative effect on adipocyte maturity and adipocyte-specific processes like lipolysis.

physiology↗