Mika Tan Resume Anal-ysis
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Although protein aggregation is primarily associated with loss of function and toxicity, it is also known to increase bacterial survival under stress conditions. Indeed, protein aggregation not only helps bacteria cope with proteotoxic stress such as heat shock or oxidative stress, but a growing body of research shows that it also improves survival during antibiotic treatment by inducing dormancy. A well-known example of inactive cells are persisters, which are temporarily resistant to the effects of antibiotics. These persister cells can switch back to a sensitive state and resume growth when antibiotics are not used, and are therefore considered an important cause of recurrent infections. Increasing evidence suggests that this antibiotic-resistant persistence state is closely related to, or possibly even contributes to, protein aggregation. In addition, another dormant bacterial phenotype, the viable but noncultivable (VBNC) state, was also shown to be associated with aggregation. These results suggest that persisters and VBNC cells may form different stages of the same sleep program caused by progressive protein aggregation. In this mini review, we discuss the relationship between aggregation and bacterial dormancy, focusing on both persisters and VBNC cells. Understanding the link between protein aggregation and dormancy will not only provide insight into the basics of bacterial survival, but could also prove invaluable in our future fight against them.
Mika Tan Resume Anal-ysis
Antibiotic treatment failure has become a worldwide problem due to the proliferation and spread of various bacterial survival mechanisms. One way bacteria can survive antibiotic treatment is by becoming resistant as a result of genetic changes that allow the bacteria to multiply in the presence of the antibiotic, such as by promoting drug efflux, altering the antibiotic’s target, or directly inactivating the antibiotic (Reygaert). , 2018). In addition to surviving antibiotics by acquiring genetic resistance, cells can also defend themselves without acquiring inherited genetic changes. An example of such a non-genetic antibiotic survival mechanism is becoming inactive. Dormant cells are characterized by lower metabolism and lack of growth (Lennon and Jones, 2011). Because antibiotics require active targets (Eng et al., 1991), shutting down some important pathways is thought to prevent the damaging effects of antibiotics, thereby promoting tolerance (Hu and Coates, 2012; Balaban et al., 2019). A well-known example of inactive cells are persisters. Persisters form a small, genetically identical subpopulation of bacteria that are temporarily resistant to antibiotics. They cannot grow in the presence of an antibiotic, but can withstand antibiotic pressure while in a persistent state. These persistent cells are most often thought to survive antibiotic treatment by becoming dormant, for example by lowering ATP levels and inhibiting important macromolecular processes such as transcription and translation (Dewachter et al., 2019; Wilmaerts et al., 2019b). However, persistence is also sporadically associated with active mechanisms such as antibiotic efflux pumps and DNA repair (Nguyen et al., 2011; Orman and Brynildsen, 2013a; Völzing and Brynildsen, 2015; Pu et al., 2016). Despite being dormant, resistant animals can easily resume growth when antibiotics are withdrawn (Balaban et al., 2019; Wilmaerts et al., 2019a). This regrowth is related to the chronic nature of the infections (Dhar and McKinney, 2010; Mulcahy et al., 2010; Goneau et al., 2014; Schumacher et al., 2015).
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In addition to persistence, other dormant bacterial phenotypes exist, such as the viable but noncultivable (VBNC) state (Xu et al., 1982). VBNC cells remain metabolically active, but have lost the ability to grow in standard media that would otherwise support their proliferation (Oliver, 1993). This quiescent state protects VBNC cells from antibiotics and other stresses (Nowakowska and Oliver, 2013). Contrary to persisters, VBNC cells do not resume growth when provided with fresh medium, but instead require a specific factor to revive (Li et al., 2014). Although these resuscitation factors are not always known (Yamamoto, 2000), it appears that at least some VBNC cells can be resuscitated in vivo (Colwell et al., 1996) and induce recurrent infections (Pai et al., 2000; Rivers and Steck, 2001).
Despite their different survival, persisters and VBNC cells also share some common characteristics. They are both resistant to antibiotics (Nowakowska and Oliver, 2013; Balaban et al., 2019) and are in a dormant state with no growth or slow growth (Xu et al., 1982; Balaban et al., 2004), low metabolism. (Shleeva et al., 2004; Amato et al., 2014), and reduced energy production (Dörr et al., 2010; Verstraeten et al., 2015; Zhao et al., 2016). In addition, persisters and VBNC cells also share similarities in their formation, suggesting a link between them. Persisters and VBNC cells can be generated stochastically in unstressed exponential phase cultures (Balaban et al., 2004; Orman and Brynildsen, 2013b). However, they are more often caused by environmental stress. Some examples of stress that induce both inactive phenotypes are nutrient (Betts et al., 2002; Mishra et al., 2012), oxidative (Wu et al., 2012; Li et al., 2014), osmotic (Roth et al. ., 1988; Murakami et al., 2005), acid (Cunningham et al., 2009; Hong W. et al., 2012) and temperature stress (Oliver et al., 1991; Cardoso et al., 2010). Furthermore, both persistence and VBNC status have been linked to the general stress response (Boaretti et al., 2003; Murakami et al., 2005), toxin and antitoxin modules (Moyed and Bertrand, 1983; Korch and Hill, 2006), and protein aggregation ( Leszczynska et al., 2013; Mordukhova and Pan, 2014; Pu et al., 2019; Yu et al., 2019; Cesar et al., 2020; Dewachter et al., 2021; Huemer et al., 2021 ). Thus, persistent and VBNC cells share many similarities. It is therefore hypothesized that they represent different stages of the same sleep program with different depths of rest; natura and VBNC cells are in shallow and deep sleep states, respectively (Li et al., 2014; Ayrapetyan et al., 2015; Kim et al., 2018; Pu et al., 2019; Dewachter et al., 2021).
Recently, experimental support for this hypothesis has emerged, showing that both persistence and the VBNC state are associated with protein aggregation and that progressive aggregation can drive development from persistence to the VBNC state (Figure 1) (Pu et al., 2019; Dewachter et al. et al., 2021). Indeed, previous work has also shown a link between aggregation and persistence (Leszczynska et al., 2013; Mordukhova and Pan, 2014; Pu et al., 2019; Yu et al., 2019; Dewachter et al., 2021; Huemer et al., 2019). ., 2021). In this review, we take a closer look at the ever-increasing number of studies linking protein aggregation and persistence. In addition, we discuss how aggregation in general might induce sleepiness.
Figure 1. A model depicting the role of protein aggregation in quiescent cell formation and awakening. Progressive protein aggregation is suggested to trigger the switch from sensitive to inactive cells. Aggregation can lead to a transition from sensitive cells to a shallow inactive persistent state. Further development of aggregates may lead to a transition from persistent cells to a deeper inactive VBNC state. This aggregation-induced dormancy makes the cells resistant to antibiotics. This tolerance is probably caused by the sequestration of proteins in the cell, thereby shutting down various important cellular pathways. To wake up again, these dormant cells may first need to remove aggregates. Bacteria use chaperones to do this splitting.
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For a cell, the amount of protein that takes over the natural state is essential because only properly folded proteins function properly. This amount depends on the balance between the rate of translation, the rate of protein folding, and the stability of that fold (Sabate et al., 2010). If this balance is disturbed, proteins can unfold or misfold, causing their aggregation-prone regions to be exposed. These aggregation-prone regions are hydrophobic stretches that cause protein aggregation when exposed (Rousseau et al., 2006). They do this by interacting with aggregation-prone regions of other non-native proteins and forming intermolecular β-sheets in a dose-dependent manner (Bednarska et al., 2013).
Two different classes of protein aggregates exist: amyloid and amorphous aggregates (Figure 2). In amyloid aggregates, the intermolecular β-sheets are perpendicular to the central axis of the aggregate, which gives them a highly ordered structure (Sunde and Blake, 1997). Amorphous aggregates or inclusion bodies exist alongside amyloids. These amorphous aggregates also contain some amyloid-like β structures, but lack long-range order. This makes them unstructured in electron microscopic images (Wang et al., 2008).
Figure 2. Different types of protein aggregations. When proteins are at least partially folded or misfolded, they can expose their aggregation-prone regions (APRs). The interaction of different protein APRs results in the formation of intermolecular β-sheets that lead to aggregation. Amyloid aggregates are highly ordered because their β-sheets are perpendicular to the central axis of the aggregate. Amorphous aggregates also contain some β structures but lack this long-range order.
The presence of amorphous or amyloid aggregates is often associated with deleterious consequences, such as loss of function of the aggregated proteins (Chiti and Dobson, 2006). Under extreme conditions of proteome-wide aggregation caused by frequent aggregation-prone regions, this widespread loss of function can even become lethal (Bednarska et al., 2015; Khodaparast et al., 2018). In addition to loss of function, amyloid aggregates are also directly implicated
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