THE LINGUISTIC REGISTER OF BRITISH PREPARATORY SCHOOLS IN ANTHONY BUCKERIDGE’S JENNINGS GOES TO SCHOOL

The unique language employed in many British Public Schools has long been noted; that of the Preparatory Schools from which the Public Schools mostly draw their pupils has generally been neglected.[1] Public School English is a feature of such popular sources as the novel Tom Brown’s Schooldays (1857) and has had formal analysis at least since 1900, the year of publication of Farmer’s Public School Word Book. By contrast, there are far fewer sources for the language of the Preparatory Schools. In Jennings Goes to School, novelist Anthony Buckeridge provides a surprisingly rich overview of this English linguistic Register as it was in the late 1940s. The Jennings Register is explored here through a Jennings word-list as an appendix to this article, and through discussion within this article of the Register in action. The Jennings Register looks in two directions. It is the primary source of Public School English and therefore of the dialect of British English associated with the Upper and Upper-Middle Classes. However, the Jennings Register surprises in that its sources are primarily Working Class and from popular culture, and in this respect it is a dialect of the Working Class. Preparatory School English therefore appears to provide a bridge between various class-based dialects of British English. It may be regarded as a linguistic and cultural unifier for Britain in the twentieth century.The structure of British Schools should perhaps be clarified. Public Schools are fee-charging schools, in contrast with State Schools which charge no fees. Public Schools include many of the most famous schools in Britain, perhaps in the world, for example Charterhouse, Eton, Harrow, Merchant Taylors’, Rugby, St Paul’s, Shrewsbury, Westminster and Winchester. Most are boarding schools, most were for boys only, and most provide education for ages 13-18. Fee-charging schools for the age range of (typically) 8-13 are called Preparatory Schools, and these are schools which prepare pupils for entry to the Public Schools

Arthur Ransome and the Dialect of Norfolk

Arthur Ransome provides information about the dialect of the English county of Norfolk as it was actually spoken in the 1930s. Two of his novels (Coot Club and The Big Six) are set on the Norfolk Broads. In these he offers some Norfolk vocabulary within the reported speech of some of his characters, along with some direct reflection on the dialect. However his masterpiece of Norfolk dialect is within Coots in the North (his unfinished novel, not published during his lifetime) where he presents what is in effect an extended Norfolk dialogue of over two-hundred lines. Ransome was an astute observer of language, and records the Norfolk dialogue with apparent accuracy and without contrivance

HISTORICAL PERSPECTIVES ON THE DEVELOPMENT AND SPREAD OF ENGLISH

There has never been a language like English. Mother tongue to around 375 million people and second language to many hundreds of millions more, the first language of business and the internet, English is truly a world-wide language. English has a unique position as the essential language skill for the world, for it is in English that the world is communicating. It is the prime beneficiary of the world-wide communications revolution and the only language ever to have achieved global status. In recorded history – in a little over one-thousand five-hundred years - it has grown from the local dialect of a minor Germanic tribe of a few thousand people living in the north of continental Europe to become the most widespread language ever. Never before has any language achieved the status now enjoyed by English, nor could this dominance have been predicted. How English has become the global language is a natural area for enquiry

Molecular mechanisms that stabilize short term synaptic plasticity during presynaptic homeostatic plasticity.

Presynaptic homeostatic plasticity (PHP) compensates for impaired postsynaptic neurotransmitter receptor function through a rapid, persistent adjustment of neurotransmitter release, an effect that can exceed 200%. An unexplained property of PHP is the preservation of short-term plasticity (STP), thereby stabilizing activity-dependent synaptic information transfer. We demonstrate that the dramatic potentiation of presynaptic release during PHP is achieved while simultaneously maintaining a constant ratio of primed to super-primed synaptic vesicles, thereby preserving STP. Mechanistically, genetic, biochemical and electrophysiological evidence argue that a constant ratio of primed to super-primed synaptic vesicles is achieved by the concerted action of three proteins: Unc18, Syntaxin1A and RIM. Our data support a model based on the regulated availability of Unc18 at the presynaptic active zone, a process that is restrained by Syntaxin1A and facilitated by RIM. As such, regulated vesicle priming/super-priming enables PHP to stabilize both synaptic gain and the activity-dependent transfer of information at a synapse

Dual separable feedback systems govern firing rate homeostasis.

Firing rate homeostasis (FRH) stabilizes neural activity. A pervasive and intuitive theory argues that a single variable, calcium, is detected and stabilized through regulatory feedback. A prediction is that ion channel gene mutations with equivalent effects on neuronal excitability should invoke the same homeostatic response. In agreement, we demonstrate robust FRH following either elimination of Kv4/Shal protein or elimination of the Kv4/Shal conductance. However, the underlying homeostatic signaling mechanisms are distinct. Eliminating Shal protein invokes Krüppel-dependent rebalancing of ion channel gene expression including enhanced slo, Shab, and Shaker. By contrast, expression of these genes remains unchanged in animals harboring a CRISPR-engineered, Shal pore-blocking mutation where compensation is achieved by enhanced IKDR. These different homeostatic processes have distinct effects on homeostatic synaptic plasticity and animal behavior. We propose that FRH includes mechanisms of proteostatic feedback that act in parallel with activity-driven feedback, with implications for the pathophysiology of human channelopathies

VCP-dependent muscle degeneration is linked to defects in a dynamic tubular lysosomal network in vivo.

Lysosomes are classically viewed as vesicular structures to which cargos are delivered for degradation. Here, we identify a network of dynamic, tubular lysosomes that extends throughout Drosophila muscle, in vivo. Live imaging reveals that autophagosomes merge with tubular lysosomes and that lysosomal membranes undergo extension, retraction, fusion and fission. The dynamics and integrity of this tubular lysosomal network requires VCP, an AAA-ATPase that, when mutated, causes degenerative diseases of muscle, bone and neurons. We show that human VCP rescues the defects caused by loss of Drosophila VCP and overexpression of disease relevant VCP transgenes dismantles tubular lysosomes, linking tubular lysosome dysfunction to human VCP-related diseases. Finally, disruption of tubular lysosomes correlates with impaired autophagosome-lysosome fusion, increased cytoplasmic poly-ubiquitin aggregates, lipofuscin material, damaged mitochondria and impaired muscle function. We propose that VCP sustains sarcoplasmic proteostasis, in part, by controlling the integrity of a dynamic tubular lysosomal network

Mechanisms of Synapse Assembly and Disassembly

AbstractThe mechanisms that govern synapse formation and elimination are fundamental to our understanding of neural development and plasticity. The wiring of neural circuitry requires that vast numbers of synapses be formed in a relatively short time. The subsequent refinement of neural circuitry involves the formation of additional synapses coincident with the disassembly of previously functional synapses. There is increasing evidence that activity-dependent plasticity also involves the formation and disassembly of synapses. While we are gaining insight into the mechanisms of both synapse assembly and disassembly, we understand very little about how these phenomena are related to each other and how they might be coordinately controlled to achieve the precise patterns of synaptic connectivity in the nervous system. Here, we review our current understanding of both synapse assembly and disassembly in an effort to unravel the relationship between these fundamental developmental processes

MCTP is an ER-resident calcium sensor that stabilizes synaptic transmission and homeostatic plasticity.

Presynaptic homeostatic plasticity (PHP) controls synaptic transmission in organisms from Drosophila to human and is hypothesized to be relevant to the cause of human disease. However, the underlying molecular mechanisms of PHP are just emerging and direct disease associations remain obscure. In a forward genetic screen for mutations that block PHP we identified mctp (Multiple C2 Domain Proteins with Two Transmembrane Regions). Here we show that MCTP localizes to the membranes of the endoplasmic reticulum (ER) that elaborate throughout the soma, dendrites, axon and presynaptic terminal. Then, we demonstrate that MCTP functions downstream of presynaptic calcium influx with separable activities to stabilize baseline transmission, short-term release dynamics and PHP. Notably, PHP specifically requires the calcium coordinating residues in each of the three C2 domains of MCTP. Thus, we propose MCTP as a novel, ER-localized calcium sensor and a source of calcium-dependent feedback for the homeostatic stabilization of neurotransmission

A postsynaptic PI3K-cII dependent signaling controller for presynaptic homeostatic plasticity.

Presynaptic homeostatic plasticity stabilizes information transfer at synaptic connections in organisms ranging from insect to human. By analogy with principles of engineering and control theory, the molecular implementation of PHP is thought to require postsynaptic signaling modules that encode homeostatic sensors, a set point, and a controller that regulates transsynaptic negative feedback. The molecular basis for these postsynaptic, homeostatic signaling elements remains unknown. Here, an electrophysiology-based screen of the Drosophila kinome and phosphatome defines a postsynaptic signaling platform that includes a required function for PI3K-cII, PI3K-cIII and the small GTPase Rab11 during the rapid and sustained expression of PHP. We present evidence that PI3K-cII localizes to Golgi-derived, clathrin-positive vesicles and is necessary to generate an endosomal pool of PI(3)P that recruits Rab11 to recycling endosomal membranes. A morphologically distinct subdivision of this platform concentrates postsynaptically where we propose it functions as a homeostatic controller for retrograde, trans-synaptic signaling

A postsynaptic Spectrin scaffold defines active zone size, spacing, and efficacy at the Drosophila neuromuscular junction

Synaptic connections are established with characteristic, cell type–specific size and spacing. In this study, we document a role for the postsynaptic Spectrin skeleton in this process. We use transgenic double-stranded RNA to selectively eliminate α-Spectrin, β-Spectrin, or Ankyrin. In the absence of postsynaptic α- or β-Spectrin, active zone size is increased and spacing is perturbed. In addition, subsynaptic muscle membranes are significantly altered. However, despite these changes, the subdivision of the synapse into active zone and periactive zone domains remains intact, both pre- and postsynaptically. Functionally, altered active zone dimensions correlate with an increase in quantal size without a change in presynaptic vesicle size. Mechanistically, β-Spectrin is required for the localization of α-Spectrin and Ankyrin to the postsynaptic membrane. Although Ankyrin is not required for the localization of the Spectrin skeleton to the neuromuscular junction, it contributes to Spectrin-mediated synapse development. We propose a model in which a postsynaptic Spectrin–actin lattice acts as an organizing scaffold upon which pre- and postsynaptic development are arranged