Experimental investigation of the transition between Autler-Townes splitting and electromagnetically-induced-transparency models

Two phenomena can affect the transmission of a probe field through an absorbing medium in the presence of an additional field: electromagnetically induced transparency (EIT) and Autler-Townes splitting (ATS). Being able to discriminate between the two i

TAp73 is a central transcriptional regulator of airway multiciliogenesis.

Motile multiciliated cells (MCCs) have critical roles in respiratory health and disease and are essential for cleaning inhaled pollutants and pathogens from airways. Despite their significance for human disease, the transcriptional control that governs multiciliogenesis remains poorly understood. Here we identify TP73, a p53 homolog, as governing the program for airway multiciliogenesis. Mice with TP73 deficiency suffer from chronic respiratory tract infections due to profound defects in ciliogenesis and complete loss of mucociliary clearance. Organotypic airway cultures pinpoint TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of MCC progenitors. Mechanistically, cross-species genomic analyses and complete ciliary rescue of knockout MCCs identify TAp73 as the conserved central transcriptional integrator of multiciliogenesis. TAp73 directly activates the key regulators FoxJ1, Rfx2, Rfx3, and miR34bc plus nearly 50 structural and functional ciliary genes, some of which are associated with human ciliopathies. Our results position TAp73 as a novel central regulator of MCC differentiation

Nonlinearity and Topology

The interplay of nonlinearity and topology results in many novel and emergent properties across a number of physical systems such as chiral magnets, nematic liquid crystals, Bose-Einstein condensates, photonics, high energy physics, etc. It also results in a wide variety of topological defects such as solitons, vortices, skyrmions, merons, hopfions, monopoles to name just a few. Interaction among and collision of these nontrivial defects itself is a topic of great interest. Curvature and underlying geometry also affect the shape, interaction and behavior of these defects. Such properties can be studied using techniques such as, e.g. the Bogomolnyi decomposition. Some applications of this interplay, e.g. in nonreciprocal photonics as well as topological materials such as Dirac and Weyl semimetals, are also elucidated

Experimental investigation of the transition between Autler-Townes splitting and electromagnetically-induced transparency models

Paper IA_6_2 - From the session Coherent Effects (IA_6)If in general the transparency of an initially absorbing medium for a probe field is increased by the presence of a control field on an adjacent transition, two very different processes can be invoked to explain it. One of them is a quantum Fano interference between two paths in the three-level system, which occurs even at low control intensity and gives rise to electromagnetically-induced transparency (EIT), the other one is the appearance of two dressed states in the excited level at higher control intensity, corresponding to the Autler-Townes splitting (ATS). This distinction is particularly critical for instance for the implementation of slow light or optical quantum memories. In a recent paper, P. M. Anisimov, J. P. Dowling and B. C. Sanders proposed a quantitative test to objectively discerning ATS from EIT [1]. We experimentally investigated this test with cold atoms [2] and demonstrated that it is very sensitive to the specific properties of the medium. © 2013 IEEE.L. Giner, L. Veissier, B. Sparkes, A. Sheremet, A. Nicolas, O. Mishina, M. Scherman, S. Burks, I. Shomroni, D. V. Kupriyanov, P. K. Lam, E. Giacobino, J. Laura

Discriminating between the Autler-Townes splitting and the electromagnetically-induced transparency models: a tool for probing the medium properties

Paper QTh4C.3 - From the session Quantum Optics with Atoms and Molecules (QTh4C)We investigated a method that allows for objectively discerning between the Autler-Townes splitting and the electromagnetically-induced transparency models. We demonstrated the suitability of the test and additionally show its sensitivity to the medium properties.L. Giner, L. Veissier, B. Sparkes, A. Sheremet, A. Nicolas, O. Mishina, M. Scherman, S. Burks, I. Shomroni, D. V. Kupriyanov, P. K. Lam, E. Giacobino, and J. Laura

Exome sequencing is a useful diagnostic tool for complicated forms of hereditary spastic paraplegia

Hereditary spastic paraplegias constitute a heterogeneous group of neurodegenerative diseases encompassing pure and complicated forms, for which at least 52 loci and 31 causative genes have been identified. Although mutations in the SPAST gene explain approximately 40% of the pure autosomal dominant forms, molecular diagnosis can be challenging for the sporadic and recessive forms, which are often complicated and clinically overlap with a broad number of movement disorders. The validity of exome sequencing as a routine diagnostic approach in the movement disorder clinic needs to be assessed. The main goal of this study was to explore the usefulness of an exome analysis for the diagnosis of a complicated form of spastic paraplegia. Whole-exome sequencing was performed in two Spanish siblings with a neurodegenerative syndrome including upper and lower motor neuron, ocular and cerebellar signs. Exome sequencing revealed that both patients carry a novel homozygous nonsense mutation in exon 15 of the SPG11 gene (c.2678G>A; p.W893X), which was not found in 584 Spanish control chromosomes. After many years of follow-up and multiple time-consuming genetic testing, we were able to diagnose these patients by making use of whole-exome sequencing, showing that this is a cost-efficient diagnostic tool for the movement disorder specialist

Inhibition of the autophagic protein ULK1 attenuates axonal degeneration in vitro and in vivo, enhances translation, and modulates splicing

Axonal degeneration is a key and early pathological feature in traumatic and neurodegenerative disorders of the CNS. Following a focal lesion to axons, extended axonal disintegration by acute axonal degeneration (AAD) occurs within several hours. During AAD, the accumulation of autophagic proteins including Unc-51 like autophagy activating kinase 1 (ULK1) has been demonstrated, but its role is incompletely understood. Here, we study the effect of ULK1 inhibition in different models of lesion-induced axonal degeneration in vitro and in vivo. Overexpression of a dominant negative of ULK1 (ULK1.DN) in primary rat cortical neurons attenuates axotomy-induced AAD in vitro. Both ULK1.DN and the ULK1 inhibitor SBI-0206965 protect against AAD after rat optic nerve crush in vivo. ULK1.DN additionally attenuates long-term axonal degeneration after rat spinal cord injury in vivo. Mechanistically, ULK1.DN decreases autophagy and leads to an mTOR-mediated increase in translational proteins. Consistently, treatment with SBI-0206965 results in enhanced mTOR activation. ULK1.DN additionally modulates the differential splicing of the degeneration-associated genes Kif1b and Ddit3. These findings uncover ULK1 as an important mediator of axonal degeneration in vitro and in vivo, and elucidate its function in splicing, defining it as a putative therapeutic target