@article{HombergerBarquistVogel2022,
  author    = {Homberger, Christina and Barquist, Lars and Vogel, J{\"o}rg},
  title     = {Ushering in a new era of single-cell transcriptomics in bacteria},
  series = {microLife},
  volume    = {3},
  journal   = {microLife},
  doi       = {10.1093/femsml/uqac020},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-313292},
  year      = {2022},
  abstract  = {Transcriptome analysis of individual cells by single-cell RNA-seq (scRNA-seq) has become routine for eukaryotic tissues, even being applied to whole multicellular organisms. In contrast, developing methods to read the transcriptome of single bacterial cells has proven more challenging, despite a general perception of bacteria as much simpler than eukaryotes. Bacterial cells are harder to lyse, their RNA content is about two orders of magnitude lower than that of eukaryotic cells, and bacterial mRNAs are less stable than their eukaryotic counterparts. Most importantly, bacterial transcripts lack functional poly(A) tails, precluding simple adaptation of popular standard eukaryotic scRNA-seq protocols that come with the double advantage of specific mRNA amplification and concomitant depletion of rRNA. However, thanks to very recent breakthroughs in methodology, bacterial scRNA-seq is now feasible. This short review will discuss recently published bacterial scRNA-seq approaches (MATQ-seq, microSPLiT, and PETRI-seq) and a spatial transcriptomics approach based on multiplexed in situ hybridization (par-seqFISH). Together, these novel approaches will not only enable a new understanding of cell-to-cell variation in bacterial gene expression, they also promise a new microbiology by enabling high-resolution profiling of gene activity in complex microbial consortia such as the microbiome or pathogens as they invade, replicate, and persist in host tissue.},
  language  = {en}
}
@article{PetersenKuntzerFischeretal.2015,
  author    = {Petersen, Jens A. and Kuntzer, Thierry and Fischer, Dirk and von der Hagen, Maja and Veronika, Angela and Lobrinus, Johannes A. and Kress, Wolfram and Rushing, Elisabeth J. and Sinnreich, Michael and Jung, Hans H.},
  title     = {Dysferlinopathy in Switzerland: clinical phenotypes and potential founder effects},
  series = {BMC Neurology},
  volume    = {15},
  journal   = {BMC Neurology},
  number    = {182},
  doi       = {10.1186/s12883-015-0449-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-139920},
  year      = {2015},
  abstract  = {Background: Dysferlin is reduced in patients with limb girdle muscular dystrophy type 2B, Miyoshi myopathy, distal anterior compartment myopathy, and in certain Ethnic clusters. Methods: We evaluated clinical and genetic patient data from three different Swiss Neuromuscular Centers. Results: Thirteen patients from 6 non-related families were included. Age of onset was 18.8 +/- 4.3 years. In all patients, diallelic disease-causing mutations were identified in the DYSF gene. Nine patients from 3 non-related families from Central Switzerland carried the identical homozygous mutation, c.3031 + 2T>C. A possible founder effect was confirmed by haplotype analysis. Three patients from two different families carried the heterozygous mutation, c.1064_1065delAA. Two novel mutations were identified (c.2869C>T (p.Gln957Stop), c.5928G>A (p.Trp1976Stop)). Conclusions: Our study confirms the phenotypic heterogeneity associated with DYSF mutations. Two mutations (c.3031 + 2T>C, c.1064_1065delAA) appear common in Switzerland. Haplotype analysis performed on one case (c.3031 + 2T>C) suggested a possible founder effect.},
  language  = {en}
}