On the structured distance to uncontrollability

This article is concerned with the structured distance to uncontrollability of a linear time-invariant system and relates this concept to a variation of the μ-value. The developed framework is applied to derive computational expressions for the class of real perturbations as well as for Hermitian, symmetric, and skew-symmetric perturbations in a relatively simple manner. Examples demonstrate that the structured distance can differ from the standard, unstructured distance to uncontrollability by an arbitrary amount. It is also shown how systems of higher order can be addressed. © 2008 Elsevier B.V. All rights reserved

On the computation of structured singular values and pseudospectra

Structured singular values and pseudospectra play an important role in assessing the properties of a linear system under structured perturbations. This paper discusses computational aspects of structured pseudospectra for structures that admit an eigenvalue minimization characterization, including the classes of real, skew-symmetric, Hermitian, and Hamiltonian perturbations. For all these structures we develop algorithms that require O (n2) operations per grid point, combining the Schur decomposition with a Lanczos method. These algorithms form the basis of a graphical Matlab interface for plotting structured pseudospectra. © 2009 Elsevier B.V. All rights reserved

Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity.

Bloom's syndrome is a rare autosomal recessive disorder characterized by genomic instability and predisposition to cancer. BLM, the gene defective in Bloom's syndrome, encodes a 159-kDa protein possessing DNA-stimulated ATPase and ATP-dependent DNA helicase activities. We have examined mechanistic aspects of the catalytic functions of purified recombinant BLM protein. Through analyzing the effects of different lengths of DNA cofactor on ATPase activity, we provide evidence to suggest that BLM translocates along single-stranded DNA in a processive manner. The helicase reaction catalyzed by BLM protein was examined as a function of duplex DNA length. We show that BLM catalyzes unwinding of short DNA duplexes (/=259-bp). The presence of the human single-stranded DNA-binding protein (human replication protein A (hRPA)) stimulates the BLM unwinding reaction on the 259-bp partial duplex DNA substrate. Heterologous single-stranded DNA-binding proteins fail to stimulate similarly the helicase activity of BLM protein. This is the first demonstration of a functional interaction between BLM and another protein. Consistent with a functional interaction between hRPA and the BLM helicase, we demonstrate a direct physical interaction between the two proteins mediated by the 70-kDa subunit of RPA. The interactions between BLM and hRPA suggest that the two proteins function together in vivo to unwind DNA duplexes during replication, recombination, or repair

An ISS Small-Gain Theorem for General Networks

We provide a generalized version of the nonlinear small-gain theorem for the case of more than two coupled input-to-state stable (ISS) systems. For this result the interconnection gains are described in a nonlinear gain matrix and the small-gain condition requires bounds on the image of this gain matrix. The condition may be interpreted as a nonlinear generalization of the requirement that the spectral radius of the gain matrix is less than one. We give some interpretations of the condition in special cases covering two subsystems, linear gains, linear systems and an associated artificial dynamical system.Comment: 26 pages, 3 figures, submitted to Mathematics of Control, Signals, and Systems (MCSS

Wild rice

Revised March 1996

Programming of neural progenitors of the adult subependymal zone towards a glutamatergic neuron lineage by neurogenin 2

Although adult subependymal zone (SEZ) neural stem cells mostly generate GABAergic interneurons, a small progenitor population expresses the proneural gene Neurog2 and produces glutamatergic neurons. Here, we determined whether Neurog2 could respecify SEZ neural stem cells and their progeny toward a glutamatergic fate. Retrovirus-mediated expression of Neurog2 induced the glutamatergic lineage markers TBR2 and TBR1 in cultured SEZ progenitors, which differentiated into functional glutamatergic neurons. Likewise, Neurog2-transduced SEZ progenitors acquired glutamatergic neuron hallmarks in vivo. Intriguingly, they failed to migrate toward the olfactory bulb and instead differentiated within the SEZ or the adjacent striatum, where they received connections from local neurons, as indicated by rabies virus-mediated monosynaptic tracing. In contrast, lentivirus-mediated expression of Neurog2 failed to reprogram early SEZ neurons, which maintained GABAergic identity and migrated to the olfactory bulb. Our data show that NEUROG2 can program SEZ progenitors toward a glutamatergic identity but fails to reprogram their neuronal progeny.We are grateful to Ana Beltrán-Arranz and Laia Torres-Masjoan for help with monosynaptic tracing experiments. We are grateful to Dr. Magdalena Götz for support throughout the project. We acknowledge the Microscopy Core Facility of the Institute of Molecular Biology (IMB) in Mainz. This work was supported by a grant from the Wellcome Trust (206410/Z/17/Z). For the purpose of open access, the authors have applied a CC BY public copyright license to any author-accepted manuscript version arising from this submission. Furthermore, this work was supported by grants from the Deutsche Forschungsgemeinschaft to B.B. (CRC1080, project number 221828878; BE 4182 11-1, project number 357058359) and to M.S.B. (LE 4610 1, project number 450131873); the Research Initiative of the State of Rhineland-Palatinate at the Johannes Gutenberg University Mainz (ReALity) to B.B.; the Spanish Ministry of Science and Innovation (MICINN) to S.G. (grants RTI2018-099345-B-I00 and PID2021-128796OB-I00) and F.O. (PID2019-109155RB-I00 and BFU2015- 70067REDC); and the Inneruniversitäre Forschungsförderung Stufe 1 of the Universitätsmedizin Mainz to S.P. N.M. was supported by a fellowship from the Human Frontiers Science Program (LT000646/2015), W.F. by a fellowship from the China Scholarship Council, J.S.-L. by a fellowship from the UCM-Santander (CT82/20-CT83/20), and S.G. by the Ramón y Cajal Programme (RYC-2015-19185)

Rmi1 stimulates decatenation of double Holliday junctions during dissolution by Sgs1-Top3

double Holliday junction (dHJ) is a central intermediate of homologous recombination that can be processed to yield crossover or non-crossover recombination products. To preserve genomic integrity, cells possess mechanisms to avoid crossing over. We show that Saccharomyces cerevisiae Sgs1 and Top3 proteins are sufficient to migrate and disentangle a dHJ to produce exclusively non-crossover recombination products, in a reaction termed "dissolution." We show that Rmi1 stimulates dHJ dissolution at low Sgs1-Top3 protein concentrations, although it has no effect on the initial rate of Holliday junction (HJ) migration. Rmi1 serves to stimulate DNA decatenation, removing the last linkages between the repaired and template DNA molecules. Dissolution of a dHJ is a highly efficient and concerted alternative to nucleolytic resolution that prevents crossing over of chromosomes during recombinational DNA repair in mitotic cells and thereby contributes to genomic integrity