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Iyer, A. S.

Publications and source records attributed to Iyer, A. S..

2 recordsLinked to original sources

Mechanical coupling of compartments drives polarity and patterning of mouse auditory epithelium

Morphogenetic information arises from a combination of genetically encoded cellular properties and emergent cellular behaviours. The spatio-temporal implementation of this information is critical to ensure robust, reproducible tissue shapes, yet the principles underlying its organisation remain unknown. We investigated this principle using the mouse auditory epithelium, the organ of Corti (OC). OC consists of a sensory domain, which transduces sound through polar mechanosensory hair cells (HC), part of a mosaic with supporting cells (SC). On either side of the sensory domain are non-sensory domains. These domains undergo cellular rearrangements, which, together, lead to a spiral cochlea that contains planar polarised HCs. This makes the mammalian cochlea a compelling system to understand coordination across spatial scales. Using genetic and ex-vivo approaches, we found patterning of OC into sensory and non-sensory domains is associated with a combinatorial expression of adhesion molecules, which underpins OC into spatially defined compartments, enabling planar cell polarity (PCP) cues to regulate compartment-specific organisation. Through compartment-specific knockouts of the PCP protein, Vangl2, we find evidence of compartment coupling, a non-linear influence on the organisation within one compartment when cellular organisation is disrupted in another. In the OC, compartment coupling originates from vinculin-dependent junctional mechanics, coordinating cellular dynamics across spatial scales. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/613243v2_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@11d31c1org.highwire.dtl.DTLVardef@1ad85dcorg.highwire.dtl.DTLVardef@12f4a0corg.highwire.dtl.DTLVardef@1a663ab_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

Established Pseudomonas syringae pv. tomato infection disrupts immigration of leaf surface bacteria to the apoplast

Bacterial disease alters the infection court creating new niches. The apoplast is an oasis from the hardships of the leaf surface and is generally inaccessible to nonpathogenic members of the phyllosphere bacterial community. Previously, we demonstrated that Salmonella enterica immigrants to the leaf surface can both enter the apoplast and replicate due to conditions created by an established Xanthomonas hortorum pv. gardneri (Xhg) infection. Here, we have expanded our investigation of how infection changes the host by examining the effects of another water-soaking pathogen, Pseudomonas syringae pv tomato (Pst), on immigrating bacteria. We discovered that, despite causing macroscopically similar symptoms as Xhg, Pst infection disrupts S. enterica colonization of the apoplast. To determine if these effects were broadly applicable to phyllosphere bacteria, we examined the fates of immigrant Xhg and Pst arriving on an infected leaf. We found that this effect is not specific to S. enterica, but that immigrating Xhg or Pst also struggled to fully join the infecting Pst population established in the apoplast. To identify the mechanisms underlying these results, we quantified macroscopic infection symptoms, examined stomata as a pinch point of bacterial entry, and characterized aspects of interbacterial competition. While it may be considered common knowledge that hosts are fundamentally altered following infection, the mechanisms that drive these changes remain poorly understood. Here, we investigated these pathogens to reach a deeper understanding of how infection alters a host from a rarely accessible, inhabitable environment to an obtainable, habitable niche. IMPORTANCEPathogens dramatically alter the host during infection. Changes in host physical and biochemical characteristics benefit the pathogen and can reshape the composition of the bacterial community. In fact, rare members of the plant microbiota, namely bacterial human pathogens, such as Salmonella enterica, thrive in some plant infection courts. The increased success of human pathogens results from the conversion of the rarely accessible, inhabitable apoplast to an obtainable, habitable niche following infection. Here, we compared two phytopathogens, Pseudomonas syringae pv. tomato and Xanthomonas hortorum pv. gardneri within a tomato host and uncovered relevant niche changes potentially overlooked by the similarity in macroscopic symptoms. We investigated mechanisms used to reshape the host environment to the pathogens benefit and either success or failure of newly arriving immigrant bacteria. This study reveals information about bacterial disease of leaves and key changes that remodel inhospitable niches to new, conducive environments in the diseased host.

microbiology↗