TY - JOUR A1 - Galluzzi, L. A1 - Bravo-San Pedro, J. M. A1 - Vitale, I. A1 - Aaronson, S. A. A1 - Abrams, J. M. A1 - Adam, D. A1 - Alnemri, E. S. A1 - Altucci, L. A1 - Andrews, D. A1 - Annicchiarico-Petruzelli, M. A1 - Baehrecke, E. H. A1 - Bazan, N. G. A1 - Bertrand, M. J. A1 - Bianchi, K. A1 - Blagosklonny, M. V. A1 - Blomgren, K. A1 - Borner, C. A1 - Bredesen, D. E. A1 - Brenner, C. A1 - Campanella, M. A1 - Candi, E. A1 - Cecconi, F. A1 - Chan, F. K. A1 - Chandel, N. S. A1 - Cheng, E. H. A1 - Chipuk, J. E. A1 - Cidlowski, J. A. A1 - Ciechanover, A. A1 - Dawson, T. M. A1 - Dawson, V. L. A1 - De Laurenzi, V. A1 - De Maria, R. A1 - Debatin, K. M. A1 - Di Daniele, N. A1 - Dixit, V. M. A1 - Dynlacht, B. D. A1 - El-Deiry, W. S. A1 - Fimia, G. M. A1 - Flavell, R. A. A1 - Fulda, S. A1 - Garrido, C. A1 - Gougeon, M. L. A1 - Green, D. R. A1 - Gronemeyer, H. A1 - Hajnoczky, G. A1 - Hardwick, J. M. A1 - Hengartner, M. O. A1 - Ichijo, H. A1 - Joseph, B. A1 - Jost, P. J. A1 - Kaufmann, T. A1 - Kepp, O. A1 - Klionsky, D. J. A1 - Knight, R. A. A1 - Kumar, S. A1 - Lemasters, J. J. A1 - Levine, B. A1 - Linkermann, A. A1 - Lipton, S. A. A1 - Lockshin, R. A. A1 - López-Otín, C. A1 - Lugli, E. A1 - Madeo, F. A1 - Malorni, W. A1 - Marine, J. C. A1 - Martin, S. J. A1 - Martinou, J. C. A1 - Medema, J. P. A1 - Meier, P. A1 - Melino, S. A1 - Mizushima, N. A1 - Moll, U. A1 - Muñoz-Pinedo, C. A1 - Nuñez, G. A1 - Oberst, A. A1 - Panaretakis, T. A1 - Penninger, J. M. A1 - Peter, M. E. A1 - Piacentini, M. A1 - Pinton, P. A1 - Prehn, J. H. A1 - Puthalakath, H. A1 - Rabinovich, G. A. A1 - Ravichandran, K. S. A1 - Rizzuto, R. A1 - Rodrigues, C. M. A1 - Rubinsztein, D. C. A1 - Rudel, T. A1 - Shi, Y. A1 - Simon, H. U. A1 - Stockwell, B. R. A1 - Szabadkai, G. A1 - Tait, S. W. A1 - Tang, H. L. A1 - Tavernarakis, N. A1 - Tsujimoto, Y. A1 - Vanden Berghe, T. A1 - Vandenabeele, P. A1 - Villunger, A. A1 - Wagner, E. F. A1 - Walczak, H. A1 - White, E. A1 - Wood, W. G. A1 - Yuan, J. A1 - Zakeri, Z. A1 - Zhivotovsky, B. A1 - Melino, G. A1 - Kroemer, G. T1 - Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 JF - Cell Death and Differentiation N2 - Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death. Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121207 VL - 22 ER - TY - JOUR A1 - Albrecht, Marco A1 - Sharma, Cynthia M. A1 - Dittrich, Marcus T. A1 - Müller, Tobias A1 - Reinhardt, Richard A1 - Vogel, Jörg A1 - Rudel, Thomas T1 - The Transcriptional Landscape of Chlamydia pneumoniae N2 - Background: Gene function analysis of the obligate intracellular bacterium Chlamydia pneumoniae is hampered by the facts that this organism is inaccessible to genetic manipulations and not cultivable outside the host. The genomes of several strains have been sequenced; however, very little information is available on the gene structure and transcriptome of C. pneumoniae. Results: Using a differential RNA-sequencing approach with specific enrichment of primary transcripts, we defined the transcriptome of purified elementary bodies and reticulate bodies of C. pneumoniae strain CWL-029; 565 transcriptional start sites of annotated genes and novel transcripts were mapped. Analysis of adjacent genes for cotranscription revealed 246 polycistronic transcripts. In total, a distinct transcription start site or an affiliation to an operon could be assigned to 862 out of 1,074 annotated protein coding genes. Semi-quantitative analysis of mapped cDNA reads revealed significant differences for 288 genes in the RNA levels of genes isolated from elementary bodies and reticulate bodies. We have identified and in part confirmed 75 novel putative non-coding RNAs. The detailed map of transcription start sites at single nucleotide resolution allowed for the first time a comprehensive and saturating analysis of promoter consensus sequences in Chlamydia. Conclusions: The precise transcriptional landscape as a complement to the genome sequence will provide new insights into the organization, control and function of genes. Novel non-coding RNAs and identified common promoter motifs will help to understand gene regulation of this important human pathogen. KW - Chlamydia pneumoniae Y1 - 2011 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-69116 ER - TY - JOUR A1 - Remmele, Christian W. A1 - Xian, Yibo A1 - Albrecht, Marco A1 - Faulstich, Michaela A1 - Fraunholz, Martin A1 - Heinrichs, Elisabeth A1 - Dittrich, Marcus T. A1 - Müller, Tobias A1 - Reinhardt, Richard A1 - Rudel, Thomas T1 - Transcriptional landscape and essential genes of Neisseria gonorrhoeae N2 - The WHO has recently classified Neisseria gonorrhoeae as a super-bacterium due to the rapid spread of antibiotic resistant derivatives and an overall dramatic increase in infection incidences. Genome sequencing has identified potential genes, however, little is known about the transcriptional organization and the presence of non-coding RNAs in gonococci. We performed RNA sequencing to define the transcriptome and the transcriptional start sites of all gonococcal genes and operons. Numerous new transcripts including 253 potentially non-coding RNAs transcribed from intergenic regions or antisense to coding genes were identified. Strikingly, strong antisense transcription was detected for the phase-variable opa genes coding for a family of adhesins and invasins in pathogenic Neisseria, that may have regulatory functions. Based on the defined transcriptional start sites, promoter motifs were identified. We further generated and sequenced a high density Tn5 transposon library to predict a core of 827 gonococcal essential genes, 133 of which have no known function. Our combined RNA-Seq and Tn-Seq approach establishes a detailed map of gonococcal genes and defines the first core set of essential gonococcal genes. KW - Neisseria gonorrhoeae Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-113676 ER -