Activity

Toxoplasma and other apicomplexan parasites undergo a unique form of cellular locomotion referred to as “gliding motility.” Gliding motility is crucial for parasite survival as it powers tissue dissemination, host cell invasion and egress. Distinct environmental cues lead to activation of gliding motility and have become a prominent focus of recent investigation. Progress has been made toward understanding what environmental cues are sensed and how these signals are transduced in order to regulate the machinery and cellular events powering gliding motility. In this review, we will discuss new findings and integrate these into our current understanding to propose a model of how environmental sensing is achieved to regulate gliding motility in Toxoplasma. Collectively, these findings also have implications for the understanding of gliding motility across Apicomplexa more broadly.Small-molecule plant hormones principally control plant growth, development, differentiation, and environmental responses. Nine types of plant hormones are ubiquitous in angiosperms, and the molecular mechanisms of their hormone actions have been elucidated during the last two decades by genomic decoding of model plants with genetic mutants. In particular, the discovery of hormone receptors has greatly contributed to the understanding of signal transduction systems. The three-dimensional structure of the ligand-receptor complex has been determined for eight of the nine hormones by X-ray crystal structure analysis, and ligand perception mechanisms have been revealed at the atomic level. C381 Collective research has revealed the molecular function of plant hormones that act as either molecular glue or an allosteric regulator for activation of receptors. In this review, we present an overview of the respective hormone signal transduction and describe the structural bases of ligand-receptor interactions.Teleost gill arches are exquisitely evolved to maximize foraging efficiency, and include structures for the capture, filtering, and processing of prey. While both plasticity and a genetic basis for gill arch traits have been noted, the relative contributions of genetics and the environment in shaping these structures remains poorly understood. East African cichlids are particularly useful in this line of study due to their highly diverse and plastic feeding apparatus. Here we explore the gene-by-environmental effects on cichlid GRs by rearing pure bred species and their F3 hybrids in different foraging environments. We find that anatomical differences between species are dependent on the environment. The genetic architecture of these traits is also largely distinct between foraging environments. We did, however, note a few genomic “hotspots” where multiple traits map to a common region. One of these, for GR number across multiple arches, maps to the ptch1 locus, a key component of the Hedgehog (Hh) pathway that has previously been implicated in cichlid oral jaw shape and plasticity. Since Hh signalling has not previously been implicated in GR development, we explored functional roles for this pathway. Using a small molecule inhibitor in cichlids, as well as zebrafish transgenic systems, we demonstrate that Hh levels negatively regulate GR number, and are both necessary and sufficient to maintain plasticity in this trait. In all these data underscore the critical importance of the environment in determining the relationship between genotype and phenotype, and provide a molecular inroad to better understand the origins of variation in this important foraging-related trait.

Glucocerebrosidase gene mutations are a common genetic risk factor for Parkinson’s disease. They exhibit incomplete penetrance. The objective of the present study was to measure microglial activation and dopamine integrity in glucocerebrosidase gene mutation carriers without Parkinson’s disease compared to controls.

We performed PET scans on 9 glucocerebrosidase gene mutation carriers without Parkinson’s disease and 29 age-matched controls. We measured microglial activation as

C-(R)-PK11195 binding potentials, and dopamine terminal integrity with

F-dopa influx constants.

The

C-(R)-PK11195 binding potential was increased in the substantia nigra of glucocerebrosidase gene carriers compared with controls (Student t test; right, t = -4.45, P = 0.0001). Statistical parametric mapping also localized significantly increased

C-(R)-PK11195 binding potential in the occipital and temporal lobes, cerebellum, hippocampus, and mesencephalon. The degree of hyposmia correlated with nigral

C-(R)-PK11195 regional binding potentials (Spearman’s rank, P = 0.0066). Mean striatal

F-dopa uptake was similar to healthy controls.

In vivo

C-(R)-PK11195 PET imaging detects neuroinflammation in brain regions susceptible to Lewy pathology in glucocerebrosidase gene mutation carriers without Parkinson’s. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

In vivo 11 C-(R)-PK11195 PET imaging detects neuroinflammation in brain regions susceptible to Lewy pathology in glucocerebrosidase gene mutation carriers without Parkinson’s. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.Plants have short-term stress memory that enables them to maintain the expression state of a substantial subset of heat-inducible genes during stress recovery after heat stress. Little is known about the molecular mechanisms controlling stress-responsive gene expression at the recovery stage in plants, however. In this article, we demonstrate that histone H3K4 methyltransferases SDG25 and ATX1 are required for heat-stress tolerance in Arabidopsis. SDG25 and ATX1 are not only important for stress-responsive gene expression during heat stress, but also for maintaining stress-responsive gene expression during stress recovery. A combination of whole-genome bisulfite sequencing, RNA-sequencing and ChIP-qPCR demonstrated that mutations of SDG25 and ATX1 decrease histone H3K4me3 levels, increase DNA cytosine methylation and inhibit the expression of a subset of heat stress-responsive genes during stress recovery in Arabidopsis. ChIP-qPCR results confirm that ATX1 binds to chromatins associated with these target genes.