Search

Plantain is a natural hybrid coming from interspecific crossing between two major banana species: Musa acuminata (genome A) and Musa balbisiana (genome B). All B genomes contain viral integrations of Banana streak virus (BSV), responsible for the banana streak disease, which affects plant growth and fruit production. The plantain genome (AAB) contains viral integrations of two BSV species (referred as endogenous BSV, or eBSV) and can develop eBSV-derived infections following biotic and abiotic stresses. However, no banana streak disease epidemic has been reported so far on plantain cultures. We suppose that plantain can regulate eBSV-derived infections, probably through RNA silencing acquired through the co-evolution history between B genome and BSV.During my PhD, I followed eBSV-derived infections kinetics in naturals (plantain) and artificial AAB hybrids, on whole mats and for a complete crop cycle. Virus distribution was heterogeneous across the mats, with some suckers showing severe infection while others remained un- or slightly infected. I observed viral titter fluctuations across time, with extreme cases of complete recovery in natural hybrids. Overall, average viral charge was higher in artificial hybrids compared to natural hybrids.Analysis of small virus-derived RNA profiles (from northern blots and deep sequencing) from contrasted samples taken at different stages of the infection, and from both artificial and natural hybrids are in progress. The results aiming to a better understanding of the defence mechanism involved in the infection control will be presented.

Banana streak virus (BSV) is a badnavirus infecting Musa species and inducing Banana streak disease, affecting plant growth and fruit production. BSV exists under two forms: episomal and/or integrated in host genome (referred as “endogenous BSV”, eBSV). Among these viral integrations, four BSV species (BSGFV, BSIMV, BSOLV, and BSMYV) are known to induce eBSV-derived infections under biotic and abiotic stresses.My PhD project aims to follow eBSV-derived infections kinetics in interspecific Musa hybrids (hosting eBSV sequences), over an entire crop cycle. I used qPCR as a quantitative tool to compare BSV infection between different samples, and across time. Because sequence similarity between eBSV and BSV overcomes 99%, I used relative quantification between infected and healthy samples of the same banana genotype hosting eBSV. I refer the healthy, viral particles-free samples as “calibrator”. Viral DNA amplification in the calibrator was supposed to be constant, since eBSV DNA matrix is stable. However, I observed significant variability in eBSV-DNA amplification among a large population of calibrators. This might result from transitory eBSV-DNA expresssion, not encaspidated and therefore escaping serological diagnostics.This result makes this “calibrator” system unreliable for a diagnostic purpose of low infections in banana plants having viral integrations, as standard IC-PCR (immune-capture) and RCA methods have shown better sensibility. Nevertheless, I still use this protocol in my experiments for relative quantification analysis by including a “buffer area” on both sides of the amplification baseline, reflecting viral DNA amplification variations I observed.