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This week for MicroTwJC, we look at how gut microbiota change and adapt while the gut itself is being destroyed and remade when caterpillars turn into butterflies.
When a caterpillar becomes chrysalis, it marks the beginning of an incredible transformation, which is shown in the video above. It’s internal organs change and reform, muscles break apart and reform into new shapes, and organs shift and change.
But that isn’t all that change. These caterpillars are host to a range of microbiota in its gut. The delicate balance between the host and its symbionts must be maintained. This paper investigates how this balance is maintained.
Join us next Tuesday at 8pm. Tweet into #microTwJC, and follow the discussion on Twitter, or via Tweetchat.
Link to the paper: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0086995
The majority of animals are holometabolous insects and change dramatically through development. They undergo a dramatic transformation from a larval stage, adapted to feed, to an adult separated by a pupal stage. During this pupal stage the majority of the organs are renewed including the gut. This creates a risky situation that we study here: when the gut is renewed insects risk losing beneficial microbiota while simultaneously being at risk of opportunistic infection. Here, by manipulating host and symbiont we show how host and symbiont succeed in jointly controlling opportunistic pathogens. If one or both of the partners are compromised, opportunistic pathogens dominate the gut microbiota resulting in increased mortality. These findings may be broadly applicable to insects with complete metamorphosis, including many disease vectors.
We will be back in September with a whole new modding team. Stay tuned, don’t panic, and stay science-y. More Microbiology is on the way. Mark down September 8th in your calendars.
This week on Microbiology Twitter Journal Club, we’ll be discussing a brand new broad spectrum antiviral Favipiravir, and it’s efficacy compared to Ribavirin against Mouse Norovirus.
Lethal mutagenesis has emerged as a novel potential therapeutic approach to treat viral infections. Several studies have demonstrated that increases in the high mutation rates inherent to RNA viruses lead to viral extinction in cell culture, but evidence during infections in vivo is limited. In this study, we show that the broad-range antiviral nucleoside favipiravir reduces viral load in vivo by exerting antiviral mutagenesis in a mouse model for norovirus infection. Increased mutation frequencies were observed in samples from treated mice and were accompanied with lower or in some cases undetectable levels of infectious virus in faeces and tissues. Viral RNA isolated from treated animals showed reduced infectivity, a feature of populations approaching extinction during antiviral mutagenesis. These results suggest that favipiravir can induce norovirus mutagenesis in vivo, which in some cases leads to virus extinction, providing a proof-of-principle for the use of favipiravir derivatives or mutagenic nucleosides in the clinical treatment of noroviruses.
- Is Favipiravir better than Ribavirin, and does the paper provide enough evidence for that ?
- Was the data presented clearly ?
- Do those stars above the graphs mean Christmas is coming, or something more foreboding ?
- What would you have done differently?
Join the discussion at 8pm GMT tomorrow with #MicroTwJC.
.Recently scientists have achieved a feat the like of which has not been seen in billions of years, they have added new letters to the genetic alphabet of a living organism. What did they do? How did they do it ? Is it too good to be true? All these questions, and more await.
Organisms are defined by the information encoded in their genomes, and since the origin of life this information has been encoded using a two-base-pair genetic alphabet (A–T and G–C). In vitro, the alphabet has been expanded to include several unnatural base pairs (UBPs)1, 2, 3. We have developed a class of UBPs formed between nucleotides bearing hydrophobic nucleobases, exemplified by the pair formed between d5SICS and dNaM (d5SICS–dNaM), which is efficiently PCR-amplified1 and transcribed4, 5 in vitro, and whose unique mechanism of replication has been characterized6, 7. However, expansion of an organism’s genetic alphabet presents new and unprecedented challenges: the unnatural nucleoside triphosphates must be available inside the cell; endogenous polymerases must be able to use the unnatural triphosphates to faithfully replicate DNA containing the UBP within the complex cellular milieu; and finally, the UBP must be stable in the presence of pathways that maintain the integrity of DNA. Here we show that an exogenously expressed algal nucleotide triphosphate transporter efficiently imports the triphosphates of both d5SICS and dNaM (d5SICSTP and dNaMTP) into Escherichia coli, and that the endogenous replication machinery uses them to accurately replicate a plasmid containing d5SICS–dNaM. Neither the presence of the unnatural triphosphates nor the replication of the UBP introduces a notable growth burden. Lastly, we find that the UBP is not efficiently excised by DNA repair pathways. Thus, the resulting bacterium is the first organism to propagate stably an expanded genetic alphabet.
We’ll be discussing it all at 8pm BST this Tuesday (27/05/14).
Follow the #microtwjc hashtag on Twitter to join in the discussion.
Full Paper with extended figures can be found here:
http://apinano.org.br/documentos/A-semi-synthetic-organism-with-an-expanded.pdf [edit- fixed the link- whoops!]
I hope to see you there !