Highlights d PspA, Vipp1, and ESCRT-III are members of the same polymer-forming protein family d ESCRT-III-like polymers function to remodel membranes across all domains of life d Hinges in the Vipp1 monomer enable it to form a diverse set of flexible polymers d The inner lumen of the dome-shaped Vipp1 ring binds and deforms membranes

Cell division in Streptococcus pneumoniae (pneumococcus) is performed and regulated by a protein complex consisting of at least 14 different protein elements; known as the divisome. Recent findings have advanced our understanding of the molecular events surrounding this process and have provided new understanding of the mechanisms that occur during the division of pneumococcus. This review will provide an overview of the key protein complexes and how they are involved in cell division. We will discuss the interaction of proteins in the divisome complex that underpin the control mechanisms for cell division and cell wall synthesis and remodelling that are required in S. pneumoniae, including the involvement of virulence factors and capsular polysaccharides.

␣-Tectorin (TECTA), ␤-tectorin (TECTB), and carcinoembryonic antigen-related cell adhesion molecule 16 (CEACAM) are secreted glycoproteins that are present in the tectorial membrane (TM), an extracellular structure overlying the hearing organ of the inner ear, the organ of Corti. Previous studies have shown that TECTA and TECTB are both required for formation of the striated-sheet matrix within which collagen fibrils of the TM are imbedded and that CEACAM16 interacts with TECTA. To learn more about the structural and functional significance of CEACAM16, we created a Ceacam16-null mutant mouse. In the absence of CEACAM16, TECTB levels are reduced, a clearly defined striated-sheet matrix does not develop, and Hensen's stripe, a prominent feature in the basal two-thirds of the TM in WT mice, is absent. CEACAM16 is also shown to interact with TECTB, indicating that it may stabilize interactions between TECTA and TECTB. Although brain-stem evoked responses and distortion product otoacoustic emissions are, for most frequencies, normal in young mice lacking CEACAM16, stimulus-frequency and transiently evoked emissions are larger. We also observed spontaneous otoacoustic emissions (SOAEs) in 70% of the homozygous mice. This incidence is remarkable considering that Ͻ3% of WT controls have SOAEs. The predominance of SOAEs Ͼ15 kHz correlates with the loss of Hensen's stripe. Results from mice lacking CEACAM16 are consistent with the idea that the organ of Corti evolved to maximize the gain of the cochlear amplifier while preventing large oscillations. Changes in TM structure appear to influence the balance between energy generation and dissipation such that the system becomes unstable.

The T2SS is a macromolecular complex that spans the cell envelope of many Gram-negative bacteria. It is part of a much larger superfamily of type IV filament containing systems all of which share homologous components and conserved mechanistic principles. These include the type 4a and 4b pilus (Craig et al., 2019), tight adherence (Tad) pilus (Tomich et al., 2007), mannose-sensitive hemagglutinin pilus (Marsh and Taylor, 1999), competence pilus (Piepenbrink, 2019) and archaeal T4 pilus and flagellum (Makarova et al., 2016). These systems are ancient and fundamental to both bacterial and archaeal kingdoms with phylogeny analyses suggesting a lineage split from within the last universal common ancestor (LUCA) (Denise et al., 2019). The T2SS is particularly concentrated in the Alpha-, Beta-, Gamma-and Delta-proteobacteria, as well as the Bacteroidetes and Deferribacteres (Denise et al., 2019).

Although single-trial induced long-term memories (LTM) have been of major interest in neuroscience, how LTM can form after a single episode of learning remains largely unknown. We hypothesized that the removal of molecular inhibitory constraints by microRNAs (miRNAs) plays an important role in this process. To test this hypothesis, first we constructed small non-coding RNA (sncRNA) cDNA libraries from the CNS of Lymnaea stagnalis subjected to a single conditioning trial. Then, by next generation sequencing of these libraries, we identified a specific pool of miRNAs regulated by training. Of these miRNAs, we focussed on Lym-miR-137 whose seed region shows perfect complementarity to a target sequence in the 3’ UTR of the mRNA for CREB2, a well-known memory repressor. We found that Lym-miR-137 was transiently up-regulated 1 h after single-trial conditioning, preceding a down-regulation of Lym-CREB2 mRNA. Furthermore, we discovered that Lym-miR-137 is co-expressed with Lym-CREB2 mRNA in an identified neuron with an established role in LTM. Finally, using an in vivo loss-of-function approach we demonstrated that Lym-miR-137 is required for single-trial induced LTM.