Advance online publication:

This section includes articles accepted for publication in Microbial Cell, which have not been released in a regular issue, yet. Please note that the PDF versions of advance publication articles are generally paginated starting with page 1. This does not correspond to the final pagination upon release of the issue it will appear in.

 

Microfluidic techniques for separation of bacterial cells via taxis

Jyoti P. Gurung, Murat Gel and Matthew A. B. Baker

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The microbial environment is typically within a fluid and the key processes happen at the microscopic scale where viscosity dominates over inertial forces. Microfluidic tools are thus well suited to study microbial motility because they offer precise control of spatial structures and are ideal for the generation of laminar fluid flows with low Reynolds numbers at microbial lengthscales. These tools have been used in combination with microscopy platforms to visualise and study various microbial taxes. These include establishing concentration and temperature gradients to influence motility via chemotaxis and thermotaxis, or controlling the surrounding microenvironment to influence rheotaxis, magnetotaxis, and phototaxis. Improvements in microfluidic technology have allowed fine separation of cells based on subtle differences in motility traits and have applications in synthetic biology, directed evolution, and applied medical microbiology.

PDF | Published online: 15/01/2020 | In press

Influence of delivery and feeding mode in oral fungi colonization – a systematic review

Maria Joao Azevedo, Maria de Lurdes Pereira, Ricardo Araujo, Carla Ramalho, Egija Zaura and Benedita Sampaio-Maia

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Postnatal acquisition of microorganisms from maternal and environmental sources contributes to the child microbiome development. Several studies showed that the mode of delivery and breastfeeding may have impact on the oral bacterial colonization, however, the influence on oral fungal colonization is still unknown. We performed a systematic literature review on mother to child oral fungi transmission, namely regarding the association between the mode of delivery and breastfeeding in oral yeast colonization. Our analysis revealed no significant differences between the oral mycobiome of breastfed and bottle-fed children. As for the delivery mode, the majority of studies found a relation between fungal colonization and vaginal delivery. Candida albicans was the most commonly isolated fungi species. Our analysis suggests that maternal breastfeeding does not seem to influence oral mycology, but vaginal delivery appears to promote oral yeast colonization in early life.

PDF | Published online: 07/01/2020 | In press

The euchromatic histone mark H3K36me3 preserves heterochromatin through sequestration of an acetyltransferase complex in fission yeast

Paula R. Georgescu, Matías Capella, Sabine Fischer-Burkart and Sigurd Braun

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Maintaining the identity of chromatin states requires mechanisms that ensure their structural integrity through the concerted actions of histone modifiers, readers, and erasers. Histone H3K9me and H3K27me are hallmarks of repressed heterochromatin, whereas H3K4me and H3K36me are associated with actively transcribed euchromatin. Paradoxically, several studies have reported that loss of Set2, the methyltransferase responsible for H3K36me, causes de-repression of heterochromatin. Here we show that unconstrained activity of the acetyltransferase complex Mst2C, which antagonizes heterochromatin, is the main cause of the silencing defects observed in Set2-deficient cells. As previously shown, Mst2C is sequestered to actively transcribed chromatin via binding to H3K36me3 that is recognized by the PWWP domain protein Pdp3. We demonstrate that combining deletions of set2+ and pdp3+ results in an epistatic silencing phenotype. In contrast, deleting mst2+, or other members of Mst2C, fully restores silencing in Set2-deficient cells. Suppression of the silencing defect in set2∆ cells is specific for pericentromeres and subtelomeres, which are marked by H3K9me, but is not seen for loci that lack genuine heterochromatin. Mst2 is known to acetylate histone H3K14 redundantly with the HAT Gnc5. Further, it is involved in the acetylation of the non-histone substrate and E3 ubiquitin ligase Brl1, resulting in increased H2B-K119 ubiquitylation at euchromatin. However, we reveal that none of these mechanisms are responsible for the Set2-dependent silencing pathway, implying that Mst2 targets another, unknown substrate critical for heterochromatin silencing. Our findings demonstrate that maintenance of chromatin states requires spatial constraint of opposing chromatin activities.

PDF | Published online: 03/01/2020 | In press

Viral attenuation by Endonuclease G during yeast gametogenesis: insights into ancestral roles of programmed cell death?

Jie Gao, Sabrina Chau and Marc D. Meneghini

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Viruses and other genetic parasites are present in virtually all forms of life. This chronic condition has led to diverse host cell adaptations such as CRISPR and RNAi, whose functions attenuate these parasites. It is hypothesized that programmed cell death (PCD) is an additional adaptation whose origins reside in viral defense. A core event of apoptotic PCD is the regulated release of mitochondrial inter-membrane space proteins into the cytosol, following which these apoptogenic proteins bring about the demise of the cell. The most well studied example of this is found in animals, where the release of mitochondrial cytochrome C nucleates the formation of the apoptosome, which then activates caspase mediated cell death. The release of mitochondrial proteins contributes to PCD in diverse organisms lacking the apoptosome, indicating that regulated mitochondrial release predates the evolution of canonical apoptosis. Using the budding yeast Saccharomyces cerevisiae, we recently confirmed an early study showing that Nuc1, a homolog of the mitochondrial apoptotic driver protein Endonuclease G, attenuates cytosolic double stranded RNA (dsRNA) viruses, which are endemic to yeast and many other organisms. Viral attenuation by Nuc1 occurs most prominently during meiosis and in association with its developmentally programmed relocation from the mitochondria to the cytosol. Intriguingly, meiotic viral attenuation by Nuc1 occurs within the context of meiotic PCD of the superfluous mother cell that we have also discovered. These findings are discussed here.

PDF | Published online: 17/12/2019 | In press

Depletion of SNAP-23 and Syntaxin 4 alters lipid droplet homeostasis during Chlamydia infection

Tiago Monteiro-Brás, Jordan Wesolowski and Fabienne Paumet

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Chlamydia trachomatis is an obligate intracellular pathogen that replicates inside a parasitic vacuole called the inclusion. The nascent inclusion is derived from the host plasma membrane and serves as a platform from which Chlamydia controls interactions with the host microenvironment. To survive inside the host cell, Chlamydia scavenges for nutrients and lipids by recruiting and/or fusing with various cellular compartments. The mechanisms by which these events occur are poorly understood but require host proteins such as the SNARE proteins (SNAP (Soluble N-ethylmaleimide-sensitive factor attachment protein) Receptor). Here, we show that SNAP-23 and Syntaxin 4, two plasma membrane SNAREs, are recruited to the inclusion and play an important role in Chlamydia development. Knocking down SNAP-23 and Syntaxin 4 by CRISPR-Cas9 reduces the amount of infectious progeny. We then demonstrate that the loss of both of these SNARE proteins results in the dysregulation of Chlamydia-induced lipid droplets, indicating that both SNAP-23 and Syntaxin 4 play a critical role in lipid droplet homeostasis during Chlamydia infection. Ultimately, our data highlights the importance of lipid droplets and their regulation in Chlamydia development.

PDF | Published online: 03/12/2019 | In press

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