The tissue growth controlling Hippo signalling pathway is modulated by the activity of the Casein Kinase 1 family, which regulates the protein stability of the upstream Hippo pathway component Expanded.
Nanobodies are developed that target neuronal proteins with restricted subcellular distributions and used as intrabodies to deliver cargo to specific sites within neurons and nanoscale immunolabels for improved imaging resolution.
About twenty temporal patterning genes are identified that drive an irreversible differentiation trajectory governing the heterogeneity and proliferative properties of cells in neural tumors with an early developmental origin.
DNA replication initiation proteins contain a disordered domain that impacts each stage of their function, from chromatin recruitment and initiator co-assembly to the subsequent displacement of the factors from chromatin.
The signaling ligand (p)ppGpp regulates the enzyme HPRT across species by binding to a novel class of conserved motif, yet its specificity is allosterically altered through evolution of enzyme oligomerization.
An unprecedented large-scale screen in mice for morphogenetic regulators of tissue development provides major new insights into the roles of Rho GTPases in diverse array of skin developmental processes.
Neural populations may depend on balanced recurrent connectivity to produce an efficient stimulus representation while also maintaining an accurate stimulus encoding despite the variability introduced by adapting neural responses.
Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.
The TRAIP ubiquitin ligase is required during mitosis to disassemble the replisome at sites of incomplete DNA replication, and activate the mitotic DNA repair pathway, thus preserving genome integrity.
Hairless emerged as an evolutionarily novel regulatory protein that replaced an ancestral paradigm of direct co-repressor recruitment by Suppressor of Hairless, its partner transcription factor in the Notch signaling pathway.
Proximity-labeling using engineered biotin ligases TurboID and miniTurbo enables detection of cell-type-specific and low abundance protein complexes and subcellular proteomes in Arabidopsis and other plants.
Structure-led protein engineering can expand the effector recognition profile of plant intracellular NLR immune receptors, providing a proof-of-principle for the development of novel disease resistance mechanisms in plants.
Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na+) channels.
The substrate for evolutionary divergence does not lie in changes in neuronal cell number or targeting, but rather in sensory perception and synaptic partner choice within invariant, prepatterned neuronal processes.
Genetics, in vivo imaging, and unbiased chemical biology screens reveal that Trpv6 functions as a cellular quiescence regulator and delineates a Trpv6-mediated Ca2+ signaling pathway maintaining the quiescent state.
Motor fatigability is associated with a decrease in inhibition throughout the motor network, suggesting that selective inhibitory control is a key mechanism to maintain motor efficiency during repetitive movements.
A combination of mouse genetics and biochemistry approaches reveals neurexophilin4 (Nxph4) as a context-specific α-neurexin ligand, which regulates Golgi-granule cell inhibitory synapses and motor functions.
Cells accumulate damaged proteins during aging and, by compromising the function of chaperones in folding newly synthesized G1 cyclins, proteostasis breakdown inhibits cell-cycle entry and drives yeast cells into senescence.
Transcription factors downstream of Hippo signaling control formation of the Left-Right Organizer by regulating major signaling pathways, expression of transcription factors and regulators of epigenetic programming involved in this process.
Gating currents analysis at different Ca2+ concentrations of BK channels reveals a strong allosteric coupling between Ca2+- and voltage-sensing modules via equivalent contributions exerted by the RCK1 and RCK2 Ca2+-sites.
In vivo stem cell reprogramming in the well-studied stem cell NB7-1 using the classic temporal transcription factor Hunchback increases motor neuron number and re-specifies dendritic morphology and neuromuscular synaptic partnerships.
A top-down circuit generating from the prelimbic cortex and projecting to the paraventricular nucleus of the thalamus mediates individual differences in cue-elicited responding by affecting subcortical dopamine-dependent incentive learning.
A mathematical model of bias in marker-gene and metagenomic sequencing measurements explains systematic errors in defined mixtures of microbial species, and enables quantitative and reproducible investigation of biological communities.
ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.
Viral transduction and gene manipulation of adult human brain slices will be of great value allowing investigations including therapeutic screening, electrophysiological and structural studies of properties of human CNS circuitry.
Neurons in the striatum exhibited periodic firing in monkeys attempting to detect omission of repetitive visual stimulus, while the phase of neuronal activity differed from that observed in the cerebellum.
Purkinje cells feature molecular heterogeneity that introduces differentiation in physiological properties between zebrin-identified cerebellar modules and thereby underlies the differential control on sensorimotor integration.
An in-depth metagenomic analysis of possibly the most abundant and widespread microbial lineage in the surface ocean teases apart evolutionary processes that maintain its genomic heterogeneity and biogeography.
Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.