@inbook{2922, author = {Vicente, Sara and Vladimir Kolmogorov and Rother, Carsten}, booktitle = {Markov Random Fields for Vision and Image Processing}, editor = {Blake, Andrew and Kohli, Pushmeet and Rother, Carsten}, publisher = {Massachusetts Institute of Technology Press}, title = {{Graph-cut Based Image Segmentation with Connectivity Priors}}, year = {2011}, } @inbook{2923, author = {Kumar, M Pawan and Vladimir Kolmogorov and Torr, Philip H}, booktitle = {Markov Random Fields for Vision and Image Processing}, editor = {Blake, Andrew and Kohli, Pushmeet and Rother, Carsten}, publisher = {Massachusetts Institute of Technology Press}, title = {{Analyzing Convex Relaxations for MAP Estimation}}, year = {2011}, } @inbook{2924, author = {Criminisi, Antonio and Cross, Geoffrey and Blake, Andrew and Vladimir Kolmogorov}, booktitle = {Markov Random Fields for Vision and Image Processing}, editor = {Blake, Andrew and Kohli, Pushmeet and Rother, Carsten}, publisher = {Massachusetts Institute of Technology Press}, title = {{Bilayer Segmentation of Video}}, year = {2011}, } @inbook{2925, author = {Rother, Carsten and Vladimir Kolmogorov and Boykov, Yuri and Blake, Andrew}, booktitle = {Markov Random Fields for Vision and Image Processing}, editor = {Blake, Andrew and Kohli, Pushmeet and Rother, Carsten}, publisher = {Massachusetts Institute of Technology Press}, title = {{Interactive Foreground Extraction using graph cut}}, year = {2011}, } @inbook{2935, author = {Boykov, Yuri and Vladimir Kolmogorov}, booktitle = {Markov Random Fields for Vision and Image Processing}, editor = {Blake, Andrew and Kohli, Pushmeet and Rother, Carsten}, pages = {31 -- 50}, publisher = {Massachusetts Institute of Technology Press}, title = {{Basic graph cut algorithms}}, year = {2011}, } @article{2961, abstract = {Rapid research progress in genotyping techniques have allowed large genome-wide association studies. Existing methods often focus on determining associations between single loci and a specic phenotype. However, a particular phenotype is usually the result of complex relationships between multiple loci and the environment. In this paper, we describe a two-stage method for detecting epistasis by combining the traditionally used single-locus search with a search for multiway interactions. Our method is based on an extended version of Fisher's exact test. To perform this test, a Markov chain is constructed on the space of multidimensional contingency tables using the elements of a Markov basis as moves. We test our method on simulated data and compare it to a two-stage logistic regression method and to a fully Bayesian method, showing that we are able to detect the interacting loci when other methods fail to do so. Finally, we apply our method to a genome-wide data set consisting of 685 dogs and identify epistasis associated with canine hair length for four pairs of single nucleotide polymorphisms (SNPs).}, author = {Malaspinas, Anna-Sapfo and Caroline Uhler}, journal = {Journal of Algebraic Statistics}, number = {1}, pages = {36 -- 53}, publisher = {Public Knowledge Project}, title = {{Detecting epistasis via Markov bases}}, doi = {http://dx.doi.org/10.18409/jas.v2i1.27}, volume = {2}, year = {2011}, } @inproceedings{2960, abstract = {Traditional statistical methods for the confidentiality protection for statistical databases do not scale well to deal with GWAS (genome-wide association studies) databases and external information on them. The more recent concept of differential privacy, introduced by the cryptographic community, is an approach which provides a rigorous definition of privacy with meaningful privacy guarantees in the presence of arbitrary external information. Building on such notions, we propose new methods to release aggregate GWAS data without compromising an individual's privacy. We present methods for releasing differentially private minor allele frequencies, chi-square statistics and p-values. We compare these approaches on simulated data and on a GWAS study of canine hair length involving 685 dogs. We also propose a privacy-preserving method for finding genome-wide associations based on a differentially private approach to penalized logistic regression.}, author = {Fienberg, Stephen E and Slavkovic, Aleksandra and Caroline Uhler}, publisher = {IEEE}, title = {{Privacy Preserving GWAS Data Sharing}}, doi = {10.1109/ICDMW.2011.140}, year = {2011}, } @inproceedings{2975, abstract = {Zero-knowledge proofs of knowledge (ZK-PoK) for discrete logarithms and related problems are indispensable for practical cryptographic protocols. Recently, Camenisch, Kiayias, and Yung provided a specification language (the CKY-language) for such protocols which allows for a modular design and protocol analysis: for every zero-knowledge proof specified in this language, protocol designers are ensured that there exists an efficient protocol which indeed proves the specified statement. However, the protocols resulting from their compilation techniques only satisfy the classical notion of ZK-PoK, which is not retained are when they used as building blocks for higher-level applications or composed with other protocols. This problem can be tackled by moving to the Universal Composability (UC) framework, which guarantees retention of security when composing protocols in arbitrary ways. While there exist generic transformations from $\Sigma$-protocols to UC-secure protocols, these transformation are often too inefficient for practice. In this paper we introduce a specification language akin to the CKY-language and a compiler such that the resulting protocols are UC-secure and efficient. To this end, we propose an extension of the UC-framework addressing the issue that UC-secure zero-knowledge proofs are by definition proofs of knowledge, and state a special composition theorem which allows one to use the weaker -- but more efficient and often sufficient -- notion of proofs of membership in the UC-framework. We believe that our contributions enable the design of practically efficient protocols that are UC-secure and thus themselves can be used as building blocks.}, author = {Camenisch, Jan and Stephan Krenn and Shoup, Victor}, editor = {Lee, Dong Hoon and Wang, Xiaoyun}, pages = {449 -- 467}, publisher = {Springer}, title = {{A Framework for Practical Universally Composable Zero-Knowledge Protocols}}, doi = {10.1007/978-3-642-25385-0}, volume = {7073}, year = {2011}, } @inproceedings{2977, abstract = {Cryptographic two-party protocols are used ubiquitously in everyday life. While some of these protocols are easy to understand and implement (e.g., key exchange or transmission of encrypted data), many of them are much more complex (e.g., e-banking and e-voting applications, or anonymous authentication and credential systems). For a software engineer without appropriate cryptographic skills the implementation of such protocols is often difficult, time consuming and error-prone. For this reason, a number of compilers supporting programmers have been published in recent years. However, they are either designed for very specific cryptographic primitives (e.g., zero-knowledge proofs of knowledge), or they only offer a very low level of abstraction and thus again demand substantial mathematical and cryptographic skills from the programmer. Finally, some of the existing compilers do not produce executable code, but only metacode which has to be instantiated with mathematical libraries, encryption routines, etc. before it can actually be used. In this paper we present a cryptographically aware compiler which is equally useful to cryptographers who want to benchmark protocols designed on paper, and to programmers who want to implement complex security sensitive protocols without having to understand all subtleties. Our tool offers a high level of abstraction and outputs well-structured and documented Java code. We believe that our compiler can contribute to shortening the development cycles of cryptographic applications and to reducing their error-proneness.}, author = {Bangerter, Endre and Stephan Krenn and Seifriz, Martial and Ultes-Nitsche, Ulrich}, editor = {Venter, Hein S. and Coetzee, Marijke and Loock, Marianne}, publisher = {IEEE}, title = {{cPLC - A Cryptographic Programming Language and Compiler}}, doi = {10.1109/ISSA.2011.6027533}, year = {2011}, } @inproceedings{2976, abstract = {Side channel attacks on cryptographic systems exploit information gained from physical implementations rather than theoretical weaknesses of a scheme. In recent years, major achievements were made for the class of so called access-driven cache attacks. Such attacks exploit the leakage of the memory locations accessed by a victim process. In this paper we consider the AES block cipher and present an attack which is capable of recovering the full secret key in almost realtime for AES-128, requiring only a very limited number of observed encryptions. Unlike previous attacks, we do not require any information about the plaintext (such as its distribution, etc.). Moreover, for the first time, we also show how the plaintext can be recovered without having access to the ciphertext at all. It is the first working attack on AES implementations using compressed tables. There, no efficient techniques to identify the beginning of AES rounds is known, which is the fundamental assumption underlying previous attacks. We have a fully working implementation of our attack which is able to recover AES keys after observing as little as 100 encryptions. It works against the OpenSSL 0.9.8n implementation of AES on Linux systems. Our spy process does not require any special privileges beyond those of a standard Linux user. A contribution of probably independent interest is a denial of service attack on the task scheduler of current Linux systems (CFS), which allows one to observe (on average) every single memory access of a victim process.}, author = {Gullasch, David and Bangerter, Endre and Stephan Krenn}, pages = {490 -- 505}, publisher = {IEEE}, title = {{Cache Games - Bringing Access-Based Cache Attacks on AES to Practice}}, doi = {10.1109/SP.2011.22}, year = {2011}, } @article{3092, abstract = {The phytohormone auxin is vital to plant growth and development. A unique property of auxin among all other plant hormones is its cell-to-cell polar transport that requires activity of polarly localized PIN-FORMED (PIN) auxin efflux transporters. Despite the substantial molecular insight into the cellular PIN polarization, the mechanistic understanding for developmentally and environmentally regulated PIN polarization is scarce. The long-standing belief that auxin modulates its own transport by means of a positive feedback mechanism has inspired both experimentalists and theoreticians for more than two decades. Recently, theoretical models for auxin-dependent patterning in plants include the feedback between auxin transport and the PIN protein localization. These computer models aid to assess the complexity of plant development by testing and predicting plausible scenarios for various developmental processes that occur in planta. Although the majority of these models rely on purely heuristic principles, the most recent mechanistic models tentatively integrate biologically testable components into known cellular processes that underlie the PIN polarity regulation. The existing and emerging computational approaches to describe PIN polarization are presented and discussed in the light of recent experimental data on the PIN polar targeting.}, author = {Wabnik, Krzysztof T and Govaerts, Willy and Friml, Jirí and Kleine Vehn, Jürgen}, journal = {Molecular BioSystems}, number = {8}, pages = {2352 -- 2359}, publisher = {Royal Society of Chemistry}, title = {{Feedback models for polarized auxin transport: An emerging trend}}, doi = {10.1039/c1mb05109a}, volume = {7}, year = {2011}, } @article{3089, abstract = {The phytohormone auxin is an important determinant of plant development. Directional auxin flow within tissues depends on polar localization of PIN auxin transporters. To explore regulation of PIN-mediated auxin transport, we screened for suppressors of PIN1 overexpression (supo) and identified an inositol polyphosphate 1-phosphatase mutant (supo1), with elevated inositol trisphosphate (InsP 3) and cytosolic Ca 2+ levels. Pharmacological and genetic increases in InsP 3 or Ca 2+ levels also suppressed the PIN1 gain-of-function phenotypes and caused defects in basal PIN localization, auxin transport and auxin-mediated development. In contrast, the reductions in InsP 3 levels and Ca 2+ signaling antagonized the effects of the supo1 mutation and disrupted preferentially apical PIN localization. InsP 3 and Ca 2+ are evolutionarily conserved second messengers involved in various cellular functions, particularly stress responses. Our findings implicate them as modifiers of cell polarity and polar auxin transport, and highlight a potential integration point through which Ca 2+ signaling-related stimuli could influence auxin-mediated development.}, author = {Zhang, Jing and Vanneste, Steffen and Brewer, Philip B and Michniewicz, Marta and Peter Grones and Kleine-Vehn, Jürgen and Löfke, Christian and Teichmann, Thomas and Bielach, Agnieszka and Cannoot, Bernard and Hoyerová, Klára and Xu Chen and Xue, Hong-Wei and Eva Benková and Zažímalová, Eva and Jirí Friml}, journal = {Developmental Cell}, number = {6}, pages = {855 -- 866}, publisher = {Cell Press}, title = {{Inositol trisphosphate-induced ca^2+ signaling modulates auxin transport and pin polarity}}, doi = {10.1016/j.devcel.2011.05.013}, volume = {20}, year = {2011}, } @article{3090, abstract = {The polarized transport of the phytohormone auxin [1], which is crucial for the regulation of different stages of plant development [2, 3], depends on the asymmetric plasma membrane distribution of the PIN-FORMED (PIN) auxin efflux carriers [4, 5]. The PIN polar localization results from clathrin-mediated endocytosis (CME) from the plasma membrane and subsequent polar recycling [6]. The Arabidopsis genome encodes two groups of dynamin-related proteins (DRPs) that show homology to mammalian dynamin - a protein required for fission of endocytic vesicles during CME [7, 8]. Here we show by coimmunoprecipitation (coIP), bimolecular fluorescence complementation (BiFC), and Förster resonance energy transfer (FRET) that members of the DRP1 group closely associate with PIN proteins at the cell plate. Localization and phenotypic analysis of novel drp1 mutants revealed a requirement for DRP1 function in correct PIN distribution and in auxin-mediated development. We propose that rapid and specific internalization of PIN proteins mediated by the DRP1 proteins and the associated CME machinery from the cell plate membranes during cytokinesis is an important mechanism for proper polar PIN positioning in interphase cells.}, author = {Mravec, Jozef and Petrášek, Jan and Li, Na and Boeren, Sjef and Karlova, Rumyana and Kitakura, Saeko and Pařezová, Markéta and Naramoto, Satoshi and Nodzyński, Thomasz and Dhonukshe, Pankaj and Bednarek, Sebastian Y and Zažímalová, Eva and De Vries, Sacco and Jirí Friml}, journal = {Current Biology}, number = {12}, pages = {1055 -- 1060}, publisher = {Cell Press}, title = {{Cell plate restricted association of DRP1A and PIN proteins is required for cell polarity establishment in arabidopsis}}, doi = {10.1016/j.cub.2011.05.018}, volume = {21}, year = {2011}, } @article{3088, abstract = {Background: Whereas the majority of animals develop toward a predetermined body plan, plants show iterative growth and continually produce new organs and structures from actively dividing meristems. This raises an intriguing question: How are these newly developed organs patterned? In Arabidopsis embryos, radial symmetry is broken by the bisymmetric specification of the cotyledons in the apical domain. Subsequently, this bisymmetry is propagated to the root promeristem. Results: Here we present a mutually inhibitory feedback loop between auxin and cytokinin that sets distinct boundaries of hormonal output. Cytokinins promote the bisymmetric distribution of the PIN-FORMED (PIN) auxin efflux proteins, which channel auxin toward a central domain. High auxin promotes transcription of the cytokinin signaling inhibitor AHP6, which closes the interaction loop. This bisymmetric auxin response domain specifies the differentiation of protoxylem in a bisymmetric pattern. In embryonic roots, cytokinin is required to translate a bisymmetric auxin response in the cotyledons to a bisymmetric vascular pattern in the root promeristem. Conclusions: Our results present an interactive feedback loop between hormonal signaling and transport by which small biases in hormonal input are propagated into distinct signaling domains to specify the vascular pattern in the root meristem. It is an intriguing possibility that such a mechanism could transform radial patterns and allow continuous vascular connections between other newly emerging organs.}, author = {Bishopp, Anthony and Help, Hanna and El-Showk, Sedeer and Weijers, Dolf and Scheres, Ben and Jirí Friml and Eva Benková and Mähönen, Ari Pekka and Helariutta, Ykä}, journal = {Current Biology}, number = {11}, pages = {917 -- 926}, publisher = {Cell Press}, title = {{A mutually inhibitory interaction between auxin and cytokinin specifies vascular pattern in roots}}, doi = {10.1016/j.cub.2011.04.017}, volume = {21}, year = {2011}, } @article{3093, abstract = { Plants take up iron from the soil using the IRON-REGULATED TRANSPORTER 1 (IRT1) high-affinity iron transporter at the root surface. Sophisticated regulatory mechanisms allow plants to tightly control the levels of IRT1, ensuring optimal absorption of essential but toxic iron. Here, we demonstrate that overexpression of Arabidopsis thaliana IRT1 leads to constitutive IRT1 protein accumulation, metal overload, and oxidative stress. IRT1 is unexpectedly found in trans-Golgi network/early endosomes of root hair cells, and its levels and localization are unaffected by iron nutrition. Using pharmacological approaches, we show that IRT1 cycles to the plasma membrane to perform iron and metal uptake at the cell surface and is sent to the vacuole for proper turnover. We also prove that IRT1 is monoubiquitinated on several cytosol-exposed residues in vivo and that mutation of two putative monoubiquitination target residues in IRT1 triggers stabilization at the plasma membrane and leads to extreme lethality. Together, these data suggest a model in which monoubiquitin-dependent internalization/sorting and turnover keep the plasma membrane pool of IRT1 low to ensure proper iron uptake and to prevent metal toxicity. More generally, our work demonstrates the existence of monoubiquitin-dependent trafficking to lytic vacuoles in plants and points to proteasome-independent turnover of plasma membrane proteins.}, author = {Barberon, Marie and Zelazny, Enric and Robert, Stéphanie and Conéjéro, Geneviève and Curie, Cathy and Jirí Friml and Vert, Grégory}, journal = {PNAS}, number = {32}, pages = {E450 -- E458}, publisher = {National Academy of Sciences}, title = {{Monoubiquitin dependent endocytosis of the Iron Regulated Transporter 1 IRT1 transporter controls iron uptake in plants}}, doi = {10.1073/pnas.1100659108}, volume = {108}, year = {2011}, } @article{3094, abstract = {Summary Gravitropism aligns plant growth with gravity. It involves gravity perception and the asymmetric distribution of the phytohormone auxin. Here we provide insights into the mechanism for hypocotyl gravitropic growth. We show that the Arabidopsis thaliana PIN3 auxin transporter is required for the asymmetric auxin distribution for the gravitropic response. Gravistimulation polarizes PIN3 to the bottom side of hypocotyl endodermal cells, which correlates with an increased auxin response at the lower hypocotyl side. Both PIN3 polarization and hypocotyl bending require the activity of the trafficking regulator GNOM and the protein kinase PINOID. Our data suggest that gravity-induced PIN3 polarization diverts the auxin flow to mediate the asymmetric distribution of auxin for gravitropic shoot bending.}, author = {Rakusová, Hana and Gallego-Bartolomé, Javier and Vanstraelen, Marleen and Robert, Hélène S and Alabadí, David and Blázquez, Miguel A and Eva Benková and Jirí Friml}, journal = {Plant Journal}, number = {5}, pages = {817 -- 826}, publisher = {Wiley-Blackwell}, title = {{Polarization of PIN3 dependent auxin transport for hypocotyl gravitropic response in Arabidopsis thaliana}}, doi = {10.1111/j.1365-313X.2011.04636.x}, volume = {67}, year = {2011}, } @article{3091, author = {Sauer, Michael and Friml, Jirí}, journal = {Molecular Systems Biology}, publisher = {Nature Publishing Group}, title = {{Fleeting hormone cues get stabilized for plant organogenesis}}, doi = {10.1038/msb.2011.45}, volume = {7}, year = {2011}, } @article{3102, abstract = {Multicellular organisms depend on cell production, cell fate specification, and correct patterning to shape their adult body. In plants, auxin plays a prominent role in the timely coordination of these different cellular processes. A well-studied example is lateral root initiation, in which auxin triggers founder cell specification and cell cycle activation of xylem pole–positioned pericycle cells. Here, we report that the E2Fa transcription factor of Arabidopsis thaliana is an essential component that regulates the asymmetric cell division marking lateral root initiation. Moreover, we demonstrate that E2Fa expression is regulated by the LATERAL ORGAN BOUNDARY DOMAIN18/LATERAL ORGAN BOUNDARY DOMAIN33 (LBD18/LBD33) dimer that is, in turn, regulated by the auxin signaling pathway. LBD18/LBD33 mediates lateral root organogenesis through E2Fa transcriptional activation, whereas E2Fa expression under control of the LBD18 promoter eliminates the need for LBD18. Besides lateral root initiation, vascular patterning is disrupted in E2Fa knockout plants, similarly as it is affected in auxin signaling and lbd mutants, indicating that the transcriptional induction of E2Fa through LBDs represents a general mechanism for auxin-dependent cell cycle activation. Our data illustrate how a conserved mechanism driving cell cycle entry has been adapted evolutionarily to connect auxin signaling with control of processes determining plant architecture. }, author = {Berckmans, Barbara and Vassileva, Valya and Schmid, Stephan P and Maes, Sara and Parizot, Boris and Naramoto, Satoshi and Magyar, Zoltan and Lessa Alvim Kamei, Claire and Koncz, Csaba and Bögre, Laszlo and Persiau, Geert and De Jaeger, Geert and Jirí Friml and Simon, Rüdiger and Beeckman, Tom and de Veyldera, Lieven}, journal = {Plant Cell}, number = {10}, pages = {3671 -- 3683}, publisher = {American Society of Plant Biologists}, title = {{Auxin Dependent cell cycle reactivation through transcriptional regulation of arabidopsis E2Fa by lateral organ boundary proteins}}, doi = {10.1105/tpc.111.088377}, volume = {23}, year = {2011}, } @article{3103, abstract = {Endocytosis in plants has an essential role not only for basic cellular functions but also for growth and development, hormonal signaling and communication with the environment including nutrient delivery, toxin avoidance, and pathogen defense. The major endocytic mechanism in plants depends on the coat protein clathrin. It starts by clathrin-coated vesicle formation at the plasma membrane, where specific cargoes are recognized and packaged for internalization. Recently, genetic, biochemical and advanced microscopy studies provided initial insights into mechanisms and roles of clathrin-mediated endocytosis in plants. Here we summarize the present state of knowledge and compare mechanisms of clathrin-mediated endocytosis in plants with animal and yeast paradigms as well as review plant-specific regulations and roles of this process.}, author = {Chen, Xu and Irani, Niloufer and Friml, Jirí}, journal = {Current Opinion in Plant Biology}, number = {6}, pages = {674 -- 682}, publisher = {Elsevier}, title = {{Clathrin-mediated endocytosis: The gateway into plant cells}}, doi = {10.1016/j.pbi.2011.08.006}, volume = {14}, year = {2011}, } @article{3147, abstract = {Cancer cell of origin is difficult to identify by analyzing cells within terminal stage tumors, whose identity could be concealed by the acquired plasticity. Thus, an ideal approach to identify the cell of origin is to analyze proliferative abnormalities in distinct lineages prior to malignancy. Here, we use mosaic analysis with double markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1 mutations sporadically in neural stem cells (NSCs). Surprisingly, MADM-based lineage tracing revealed significant aberrant growth prior to malignancy only in oligodendrocyte precursor cells (OPCs), but not in any other NSC-derived lineages or NSCs themselves. Upon tumor formation, phenotypic and transcriptome analyses of tumor cells revealed salient OPC features. Finally, introducing the same p53/Nf1 mutations directly into OPCs consistently led to gliomagenesis. Our findings suggest OPCs as the cell of origin in this model, even when initial mutations occur in NSCs, and highlight the importance of analyzing premalignant stages to identify the cancer cell of origin.}, author = {Liu, Chong and Sage, Jonathan C and Miller, Michael R and Verhaak, Roel G and Simon Hippenmeyer and Vogel, Hannes and Foreman, Oded and Bronson, Roderick T and Nishiyama, Akiko and Luo, Liqun and Zong, Hui}, journal = {Cell}, number = {2}, pages = {209 -- 221}, publisher = {Cell Press}, title = {{Mosaic analysis with double markers reveals tumor cell of origin in glioma}}, doi = {10.1016/j.cell.2011.06.014}, volume = {146}, year = {2011}, }