Molecular quantum spin network controlled by a single qubit

Scalable quantum technologies will require an unprecedented combination of precision and complexity for designing stable structures of well-controllable quantum systems. It is a challenging task to find a suitable elementary building block, of which a quantum network can be comprised in a scalable way. Here we present the working principle of such a basic unit, engineered using molecular chemistry, whose control and readout are executed using a nitrogen vacancy (NV) center in diamond. The basic unit we investigate is a synthetic polyproline with electron spins localized on attached molecular sidegroups separated by a few nanometers. We demonstrate the readout and coherent manipulation of very few ($\leq 6$) of these $S=1/2$ electronic spin systems and access their direct dipolar coupling tensor. Our results show, that it is feasible to use spin-labeled peptides as a resource for a molecular-qubit based network, while at the same time providing simple optical readout of single quantum states through NV-magnetometry. This work lays the foundation for building arbitrary quantum networks using well-established chemistry methods, which has many applications ranging from mapping distances in single molecules to quantum information processing.Comment: Author name typ

Alternative splicing of MALT1 controls signalling and activation of CD4+ T cells

MALT1 channels proximal T-cell receptor (TCR) signalling to downstream signalling pathways. With MALT1A and MALT1B two conserved splice variants exist and we demonstrate here that MALT1 alternative splicing supports optimal T-cell activation. Inclusion of exon7 in MALT1A facilitates the recruitment of TRAF6, which augments MALT1 scaffolding function, but not protease activity. Naive CD4+ T cells express almost exclusively MALT1B and MALT1A expression is induced by TCR stimulation. We identify hnRNP U as a suppressor of exon7 inclusion. Whereas selective depletion of MALT1A impairs T-cell signalling and activation, downregulation of hnRNP U enhances MALT1A expression and T-cell activation. Thus, TCR-induced alternative splicing augments MALT1 scaffolding to enhance downstream signalling and to promote optimal T-cell activation

Short-latency auditory projection to the frontal telencephalon of the pigeon

An auditory projection to the frontolateral telencephalon of birds, originally described by Iljitschew, is confirmed for the pigeon. Potentials evoked by acoustic stimuli were recorded from the neostriatum frontale closely surrounding the nucleus basalis, in anesthetized and awake subjects. The latency of these responses was short (5 to 8 ms) compared to that of responses recorded from the orthodox avian telencephalic auditory projection in the neostriatum caudale, field L (12 to 14 ms). The intensity and frequency sensitivities of the frontal auditory potentials, however, were similar to those of the area L responses. Clicks delivered to the auditory meati were more effective than the same stimuli directed at other parts of the head or beak. Ipsilateral and contralateral auditory stimuli were equally effective. Occlusion of the ear openings attenuated the responses; thick pasting of the remainder of the head or beak did not affect them. Trigeminal deafferentation similarly did not attenuate the frontal auditory potentials, but alblation of the cochleae totally abolished them. The hypothesis that the frontal auditory responses are due to an artifactual stimulation of trigeminal mechanoreceptors projecting to the nucleus basalis is thus rejected. The neural pathway subserving this projection and the functional role that it may play are discussed

κB-Ras Proteins Regulate Both NF-κB-Dependent Inflammation and Ral-Dependent Proliferation

The transformation of cells generally involves multiple genetic lesions that undermine control of both cell death and proliferation. We now report that κB-Ras proteins act as regulators of NF-κB and Ral pathways, which control inflammation/cell death and proliferation, respectively. Cells lacking κB-Ras therefore not only show increased NF-κB activity, which results in increased expression of inflammatory mediators, but also exhibit elevated Ral activity, which leads to enhanced anchorage-independent proliferation (AIP). κB-Ras deficiency consequently leads to significantly increased tumor growth that can be dampened by inhibiting either Ral or NF-κB pathways, revealing the unique tumor-suppressive potential of κB-Ras proteins. Remarkably, numerous human tumors show reduced levels of κB-Ras, and increasing the level of κB-Ras in these tumor cells impairs their ability to undergo AIP, thereby implicating κB-Ras proteins in human disease