2 research outputs found

    Identification of non-coding RNA interactions that dictate Staphylococcus aureus virulence

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    Staphylococcus aureus is a bacterium which has gathered much attention over the past decade due to the emergence of both antibiotic-resistant and hyper-aggressive strains. These pose a signiïŹcant threat to human health, particularly to individuals already weakened through other illnesses. When S. aureus enters the human bloodstream, it must adapt in order to survive the challenging conditions faced. In particular, it must respond to the nutritional environment of the blood which is depleted in essential cofactors such as free iron. Additionally, S. aureus must survive attacks from the host immune system which will attempt to kill the invader through phagocytes and the production of antibodies. Theworkcarriedouthereaimedtounderstandhowsmall,non-codingRNAs(sRNAs) regulate S. aureus’ adaptation to the host bloodstream. These sRNAs are typically associated with regulating the translational efïŹciency and stability of mRNAs. Through use of a technique called “UV cross-linking, ligation and sequencing of hybrids” (CLASH), I identiïŹed novel targets of many sRNAs. In particular, I studied how RsaA, an sRNA involved in membrane homeostasis, regulates the translation of a transmembrane transporter involved in antiseptic and antibiotic resistance. Additionally, I identiïŹed interactions between RsaE, an sRNA involved in metabolism, and several toxin mRNAs from the phenol-soluble modulin class. This is a novel example of the direct link between cellular metabolism and virulence. However, the most striking ïŹnding was that not only do sRNAs target mRNAs, but that they also target each other. I focused on two distinct sRNA – sRNA interactions; one between RsaA and RNAIII, and another between RsaE and RsaOG. The interaction between RsaE and RsaOG is an example of a so-called ’sponging interaction’, where RsaOG is able to antagonise the activity of RsaE. This has the effect of freeing RsaE’s targets from their regulation. I hypothesise that this ultimately induces the necessary metabolic changes required in order to survive the immediate nutritional stresses incurred after entering the bloodstream. Regarding RsaA and RNAIII, I hypothesise that this interaction is responsible for balancing virulent versus dormant behaviour. I suggest that RsaA is able to induce the destruction of RNAIII in order to steer the cell away from aggressive behaviour and into a more latent state. Additionally, the interaction between these two sRNAs also appears to operate on exquisitely short timescales, demonstrating how capable bacteria are at adapting to stresses. Ultimately, this work suggests that interactions between sRNAs are likely to be widespread and form a crucial aspect of stress responses in general. The experiments detailed herein have certainly not exhausted the produced data and I suspect that it will be utilised further in the future

    Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

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    The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & NemĂ©sio 2007; Donegan 2008, 2009; NemĂ©sio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016
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