Examplepictures of DNA-Structures
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January 01 - January 31

12 entries found

The future ..
Start date: January 08
04:00 pm 05:00 pm

Description: 

DIPP Vision Talks aim at giving insight into the research fields represented in the DIPP. They offer - from the perspective of the speaker's expertise - a significant overview of the field, including open questions, existing resources and techniques, challenges and the possible future developments.

http://www.dresden-ipp.de/curriculum/training/dipp-vision-talks/

The Dresden International PhD Program (DIPP) is jointly organized by the Dresden International Graduate School for Biomedicine and Bioengineering (DIGS-BB) and the International Max Planck Research School for Cell, Developmental and Systems Biology (IMPRS-CellDevoSys).

SRRF-Stream..
Start date: January 15
02:00 pm 03:00 pm

Description: 

SRRF-Stream workshop for super-resolved imaging

SRRF (Super-Resolution Radial Fluctuations) is an analytical approach which enables super-resolution imaging with conventional fluorophores such as GFP. Importantly, SRRF does not require high laser intensities and can therefore be used for imaging living, dynamic systems. The company ANDOR offers 'SRRF-Stream', a new real time super-resolution microscopy functionality that operates exclusively on Andor's iXon EMCCD and the new Sona back-illuminated sCMOS cameras.

The workshop begins with an introductory talk on Tuesday, while hands-on sessions take place on Wednesday at the Dragonfly High Speed Spinning Disk Microscope.

If you are interested in testing the system please contact Isabel (isabel.raabe(at)tu-dresden.de).

Tuesday, 15.1.
Talk: Andor 'SRRF-Stream' Real Time Super-Resolution for all!
Alan Mullen (ANDOR)
Time: 2 pm
Place: CRTD, left auditorium

Wednesday, 16.1.
9:00 - 12:30 Hands-on
LUNCH
13:30 - 17:00 Hands-on

Modulating ..
Start date: January 15
03:00 pm 04:00 pm

Direct in v..
Start date: January 16
02:00 pm 03:00 pm

Description: 

Abstract
Brain-resident glial cells can be directly reprogrammed into neurons in vivo by forced expression of neurogenic transcription factors. In the adult mouse cortex, such fate switch was reported to occur only following brain lesion (Heinrich et al., 2014), which is known to elicit local glial proliferation. To clarify the influence of the proliferative state of glia on the reprogramming process, we tested whether proliferative glia can be lineage converted in vivo in the absence of a prior lesion in the postnatal mouse cortex.
Glial cells proliferate locally in the early postnatal cortex (Ge et al., 2012). To target these cells for lineage conversion we injected retroviruses encoding for neurogenic transcription factors in the cortex of postnatal mice. Noticeably, overexpression of Ascl1, Neurog2 or NeuroD1 alone was inefficient in inducing glia-to-neuron conversion. We thus tested whether synergism with other molecular pathways could induce reprogramming (Gascón et al., 2016; Heinrich et al., 2014; Karow et al., 2018). Interestingly, we observed that Sox2 or Bcl2 co-expression together with Ascl1 converted glial cells into neurons, some of which expressed the inhibitory neurotransmitter GABA. Likewise, we show that Bcl2 can enhance Neurog2-mediated glia-to-neuron conversion. Remarkably, the combined expression of these two factors not only dramatically raised the conversion efficiency, but also gave rise to neurons exhibiting a highly elaborated neuronal morphology, bearing dendritic spines and developing long-distance projections. BrdU incorporation assay confirmed the proliferative state of converted cells at the time of viral infection. The functional integration and electrophysiological properties of the reprogrammed cells is currently being investigated.

This work was supported by grants of the Wellcome Trust, DFG, and BMBF (NEURON ERA-NET ImprovVision) to BB, and the Bavarian State Ministry of Education, Science and the Arts to MK. NM was supported by the Human Frontier Science Program.

Skeletal Ca..
Start date: January 18
11:00 am 12:00 pm

Precise gen..
Start date: January 18
03:00 pm 04:00 pm

Description: 

Information

Gene and base editing hold great promises in the prevention and treatment of genetic diseases. Predicting the on-target and off-target activities of Cas9/CRISPR and Base Editors is an essential requirement for a safe and efficacious treatment. Recent progress shows how the analysis and modulation of DNA repair pathway can be applied to predict base and genome editing outcomes.

  • Taheri-Ghahfarokhi, Amir, et al. "Decoding non-random mutational signatures at Cas9 targeted sites." Nucleic acids research 46.16 (2018): 8417-8434.
  • Akcakaya, Pinar, et al. "In vivo CRISPR editing with no detectable genome-wide off-target mutations." Nature 561.7723 (2018): 416.
  • Wienert, Beeke, et al. "Unbiased detection of CRISPR off-targets in vivo using DISCOVER-Seq." bioRxiv (2018): 469635.
Active torq..
Start date: January 18
04:00 pm 05:00 pm

Description: 

Lokesh Pimpale (Predoc)
"Active torque generation in the actomyosin cytoskeleton drives chiral cell arrangement."

Abstract
Most animals are left-right (LR) asymmetric, however the molecular and physical mechanisms that drive LR symmetry breaking are largely unexplored. In C. elegans LR symmetry breaking is thought to be linked to the cytoskeleton. Recently, Naganathan et al 2014, showed that the actomyosin cortex generates active chiral torques in the single cell embryo. Similar chiral flows lead to chiral cell movements that are subsequently involved in establishing the LR axis at the 6-cell stage. We speculate that chiral movements are much more prevalent in development, driving cellular rearrangements and axis repositioning. I explore these chiral morphogenetic features in a quantitative manner in early stages of worm development and determine the extent of chiral cortical flows and chiral morphogenesis in the first few divisions of the nematode. Using RNAi mediated perturbations for actomyosin regulators, I modulate chiral flows and monitor their effect on axis establishment and cellular rearrangement until the 6-cell stage. Finally, by combining thin film active chiral fluid theory with experimental data, I will deliver a physical description of how torques are generated in the actomyosin cortex and how these events lead to morphogenetic changes in development.

Jesus Eduardo Rojo Arias (Postdoc)
"A comprehensive transcription factor library for exploring cell fate conversion."

Abstract
Transcription factors (TFs) are central regulators of gene expression and cell fate. Currently, multiple cell types can be generated via enforced expression of specific TFs. Nonetheless, our understanding of TF-mediated cell conversion remains incomplete, partly due to TF abundance and diversity. To overcome this limitation, we assembled a comprehensive TF library (>1500 TFs) in an inducible antibiotic-selectable lentivirus-deliverable system. Our library represents a valuable tool for systematically exploring cell fate decisions under genetically defined conditions. We present our TF library and its application to identify TFs that rapidly and efficiently drive differentiation and neurogenesis in human induced pluripotent stem cells.

ASH Nachles..
Start date: January 19
09:00 am 02:00 pm

Resistance ..
Start date: January 25
11:00 am 12:00 pm

Description: 

Abstract

Why a given neuropathology does not impact all neurons of the same type to a similar level? This is a fascinating question in neurodegeneration research that remains unanswered.

In most neurodegenerative diseases certain neuronal subgroups degenerate fast while others, carrying the same mutations -if any-, subjected to theoretically analogous stress and displaying comparable functional properties remain unaffected, even at the latest stages of the disease. Motor neuron diseases are a group of disorders in which motor neurons (MNs) of the spinal cord and/or the motor cortex are the primary cell type affected where this perplexing feature can also be observed.

Using a variety of approaches ranging from cellular biology techniques and live imaging to genome editing and single cell genomics, and utilizing hiPSC together with transgenic animal models, we investigate the molecular mechanisms underlying such selective MN death. We devote a special focus at exploring the molecular basis of proteostasis failure -major causative event in neurodegeneration-, and at examining the contribution of cell autonomous and non-cell autonomous factors to the selective MN loss. Our ultimate goal is to understand the molecular cause of this distinctive neuronal vulnerability to design effective therapeutics targeting specific neuronal subtypes or phases of the disease.

5 most recent papers

1. Rodriguez-Muela N*, Parkhitko A, Grass T, Gibbs R, Norabuena E, Perrimon N, Singh R, Rubin LL*. Blocking p62/SQSTM1- dependent SMN degradation ameliorates the Spinal Muscular Atrophy disease phenotype. (*Corresponding authors; J Clin Invest. 2018 Jul 2;128(7):3008-3023; highlighted in "JCI This Month" for July2018 Issue, reference 95231).

2. Rodriguez-Muela N1*, Litterman NK1, Norabuena EM, Mull JL, Galazo MJ, Sun C, Ng SY, Makhortova NR, White A, Lynes MM, Chung WK, Davidow LS, Macklis JD, Rubin LL*. Single-Cell Analysis of SMN Reveals Its Broader Role in Neuromuscular Disease. Cell Reports. 2017 Feb 7;18(6):1484-1498 (*Corresponding authors, 1equal contribution).

3. Ng SY1, Soh BS1, Rodriguez-Muela N, Hendrickson DG, Price F, Rinn JL, Rubin LL. Genome-wide RNA-Seq of Human Motor Neurons Implicates Selective ER Stress Activation in Spinal Muscular Atrophy. Cell Stem Cell. 2015 Nov 5;17(5):569-84 (1equal contribution).

4. Rodríguez-Muela N, Koga H, et al.. Balance between autophagic pathways preserves retinal homeostasis. Aging Cell. 2013 Jun;12(3):478-88. (Featured on Aging Cell cover, June 2013 vol 12).

5. Rodríguez-Muela N, Germain F, et al.. Autophagy promotes survival of retinal ganglion cells after optic nerve axotomy in mice. Cell Death Differ. 2012 Jan;19(1):162-9. (Awarded "Article of the month" by SEBBM, July 2011)

Villin inte..
Start date: January 29
03:00 pm 04:00 pm

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