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8 SFB 1036 CELLULAR SURVEILLANCE AND DAMAGE RESPONSE As a consequence of the intrinsic biochemical fragility of molecules and limited robustness and precision of cellular processes, cells must routinely deal with faulty or damaged molecules and perturbations of cell physiology. Damage and erroneous processes may be tolerable or even result in some advantage eventually contributing to evolutionary diversification, but may otherwise have catastrophic consequences. Some types of damage can become encoded in the genome, and manifest as inherited or acquired diseases. Others may perturb cellular homeostasis and result in malfunction, degeneration and ageing of cells and organisms. Damage and errors are aggravated by a multitude of internal and environmental insults (stresses). Consequently, all cells, from bacteria to human, have developed a powerful network of systems, acting at multiple levels on macromolecules, cellular compartments, whole cells and entire organs, to minimize and reverse the damage that would ensue if mistakes and abnormal molecules went by unmonitored and uncorrected. The medical dimension of surveillance and damage response pathways becomes apparent when these pathways lose effective function, since this usually results in disease. The long-term goal of this Collaborative Research Center (Sonderforschungsbereich, SFB) entitled "Cellular surveillance and damage control" is to elucidate the molecular mechanisms driving and coordinating damage control systems. In 17 research projects (TP) and 2 service projects (Z) the question of how the quality of gene function is monitored and how damage signals are integrated to elicit appropriate responses will be analyzed. This should provide a comprehensive understanding of how cells react to damage and establish and maintain homeostasis. Towards this goal the SFB will investigate: Safeguarding systems that avert potential errors and damage by ensuring proper performance of cellular processes such as DNA replication, translation, and those underpinning homeostatic environments (e.g. iron homeostasis or redox state). Damage repair systems which detect damaged or abnormal macromolecules (DNA, RNA, proteins) and provide repair and/or regulated elimination. Stress response pathways that increase cellular capacity to cope with specific or global stress (e.g. heat shock, oxidative stress, protein overload in the endoplasmic reticulum). With the planned research on surveillance mechanisms and damage responses we are aiming at providing a comprehensive understanding of how cells react to damage and establish and maintain homeostasis. Participating Institutions SFB 1036 CONFERENCE PROGRAM C E L L U L A R S U R V E I L L A N C E A N D D A M A G E R E S P O N S E NETWORKS OF CELLULAR SURVEILLANCE MECHANISMS CONFERENCE 22-24 OCTOBER 2018 SFB1036 FREE ADMISSION Registration until September 15 WITH POSTER SESSION VENUE DKFZ, INF 280 Heidelberg VISIT www.zmbh.uni-heidelberg.de /sfb1036/congress_2018/ FOR MORE INFORMATION ORGANIZERS Carmen Nussbaum, Bernd Bukau, Sylvia Erhardt, Rüdiger Hell, Gislene Pereira & Aurelio Teleman SPEAKERS REUVEN AGAMI - Amsterdam, NL SIMON ALBERTI - Dresden, DE ISABEL BÄURLE - Potsdam-Golm, DE OLIVIA CASANUEVA - Cambridge, UK DON W. CLEVELAND - La Jolla, US ALLAN DRUMMOND - Chicago, US SYLVIA ERHARDT - Heidelberg, DE ANJA GROTH - Copenhagen, DK EDITH HEARD - Paris, FR MARTIN KAMPMANN - San Francisco, US GEORGIOS KARRAS - Houston, US RICHARD I. MORIMOTO - Evanston, US CARMEN NUSSBAUM - Heidelberg, DE TIAGO F. OUTEIRO - Göttingen, DE MAGDALINI POLYMENIDOU - Zurich, CH OLIVER RANDO - Worcester, US RITWICK SAWARKAR - Freiburg, DE DAVID VILCHEZ - Cologne, DE JUDITH ZAUGG - Heidelberg, DE

SFB 1036 SFB 1036 CONFERENCE ROGRAM

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SFB 1036

CELLULAR SURVEILLANCE AND DAMAGE RESPONSE

As a consequence of the intrinsic biochemical fragility of molecules and limited robustness and precision of cellular processes, cells must routinely deal with faulty or damaged molecules and perturbations of cell physiology. Damage and erroneous processes may be tolerable or even result in some advantage eventually contributing to evolutionary diversification, but may otherwise have catastrophic consequences. Some types of damage can become encoded in the genome, and manifest as inherited or acquired diseases. Others may perturb cellular homeostasis and result in malfunction, degeneration and ageing of cells and organisms. Damage and errors are aggravated by a multitude of internal and environmental insults (stresses). Consequently, all cells, from bacteria to human, have developed a powerful network of systems, acting at multiple levels on macromolecules, cellular compartments, whole cells and entire organs, to minimize and reverse the damage that would ensue if mistakes and abnormal molecules went by unmonitored and uncorrected. The medical dimension of surveillance and damage response pathways becomes apparent when these pathways lose effective function, since this usually results in disease. The long-term goal of this Collaborative Research Center (Sonderforschungsbereich, SFB) entitled "Cellular surveillance and damage control" is to elucidate the molecular mechanisms driving and coordinating damage control systems. In 17 research projects (TP) and 2 service projects (Z) the question of how the quality of gene function is monitored and how damage signals are integrated to elicit appropriate responses will be analyzed. This should provide a comprehensive understanding of how cells react to damage and establish and maintain homeostasis. Towards this goal the SFB will investigate: Safeguarding systems that avert potential errors and damage by ensuring proper performance of cellular processes such as DNA replication, translation, and those underpinning homeostatic environments (e.g. iron homeostasis or redox state). Damage repair systems which detect damaged or abnormal macromolecules (DNA, RNA, proteins) and provide repair and/or regulated elimination. Stress response pathways that increase cellular capacity to cope with specific or global stress (e.g. heat shock, oxidative stress, protein overload in the endoplasmic reticulum). With the planned research on surveillance mechanisms and damage responses we are aiming at providing a comprehensive understanding of how cells react to damage and establish and maintain homeostasis.

Participating Institutions

SFB 1036 CONFERENCE PROGRAM

CELL

ULAR

SURVEILLANCE AND DAMAGE RESPO

NSE

NE T WORKS OF

C E L LU L A RS U RV E I L L A N C EM E C H A N I S M S

CONFERENCE22-24 OCTOBER

2018

SFB1036

FREEADMISSION

Registration untilSeptember 15

WITH POSTER SESSION

VENUEDKFZ, INF 280

Heidelberg

VISITwww.zmbh.uni-heidelberg.de

/sfb1036/congress_2018/FOR MORE

INFORMATION

ORGANIZERSCarmen Nussbaum, Bernd Bukau, Sylvia Erhardt, Rüdiger Hell,Gislene Pereira & Aurelio Teleman

SPEAKERS REUVEN AGAMI - Amsterdam, NL

SIMON ALBERTI - Dresden, DEISABEL BÄURLE - Potsdam-Golm, DE

OLIVIA CASANUEVA - Cambridge, UKDON W. CLEVELAND - La Jolla, US

ALLAN DRUMMOND - Chicago, USSYLVIA ERHARDT - Heidelberg, DE

ANJA GROTH - Copenhagen, DKEDITH HEARD - Paris, FR

MARTIN KAMPMANN - San Francisco, USGEORGIOS KARRAS - Houston, US

RICHARD I. MORIMOTO - Evanston, USCARMEN NUSSBAUM - Heidelberg, DE

TIAGO F. OUTEIRO - Göttingen, DEMAGDALINI POLYMENIDOU - Zurich, CH

OLIVER RANDO - Worcester, USRITWICK SAWARKAR - Freiburg, DE

DAVID VILCHEZ - Cologne, DEJUDITH ZAUGG - Heidelberg, DE

2

Congress Venue: Deutsches Krebsforschungszentrum (DKFZ) Im Neuenheimer Feld 280 69120 Heidelberg

7

We would like to acknowledge the generous support of our sponsors:

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Day 3 (Wednesday, October 24th)

Session IV Proteostasis Regulation in Health and Disease

Chair GEORG STÖCKLIN (UMM Heidelberg University, Mannheim, DE)

9.00 – 9.30 am SIMON ALBERTI (MPI of Molecular Cell Biology and Genetics, Dresden, DE)

Molecular mechanisms controlling RNP granule dynamics and functionality

9.30 – 9.45 am ALEXANDER BUCHBERGER (Würzburg University, Würzburg, DE) ZFAND1 recruits p97 and the 26S proteasome to promote the

clearance of arsenite-induced stress granules

9.45 – 10.00 pm FABIAN DEN BRAVE (MPI for Biochemistry, Martinsried, DE) Clearance of nuclear protein aggregates by a compartment

specific Hsp40 chaperone

10.00 – 10.30 pm ALLAN DRUMMOND (University of Chicago, Chicago, US) Transient intracellular acidification regulates the core

transcriptional heat shock response

10.30 – 10.45 am CHRISTIAN MÜNCH (Goethe-University Frankfurt, Frankfurt, DE) Different mitochondrial unfolded protein response axes to

safeguard mitochondria

10.45 – 11.15 am COFFEE BREAK

Chair CLAUDIO JOAZEIRO (ZMBH Heidelberg University, Heidelberg, DE)

11.15 – 11.45 am DAVID VILCHEZ (Cologne University, Cologne, DE) Proteostasis of aging and stem cells

11.45 – 12.00 pm PARTHIVE PATEL (DKFZ, ZMBH Heidelberg University, Heidelberg, DE)

Damage sensing by a Nox-Ask1-MKK3-p38 signaling pathway mediates intestinal regeneration

12.00 – 12.30 pm MAGDALINI POLYMENIDOU (ETH Zurich, Zurich, CH) The many faces of TDP-43 aggregation 12.30 – 1.00 pm MARTIN KAMPMANN (University of California, San Francisco, US) Cellular mechanisms controlling protein aggregation and spreading in

neurodegenerative diseases

1.00 – 1.05 pm CARMEN NUSSBAUM (ZMBH Heidelberg University, DKFZ, Heidelberg, DE) - Closing remarks

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The 2nd international conference on

Networks Of Cellular Surveillance Mechanisms

in Heidelberg, Germany, October 22-24, 2018

Day 1 (Monday, October 22nd)

2.00 – 4.00 pm REGISTRATION (with coffee and light refreshments)

4.00 – 4.05 pm BERND BUKAU (ZMBH Heidelberg University, DKFZ, Heidelberg, DE) - Welcome address

Session I Key Note Session and Poster Power Show

Chair INGRID GRUMMT (DKFZ, Heidelberg, DE)

4.05 – 4.50 pm EDITH HEARD (Institut Curie Paris, FR)

Dynamics of gene expression and chromosome organisation during X-chromosome inactivation

4.50 – 5.35 pm REUVEN AGAMI (Netherlands Cancer Institute, Amsterdam, NL)

Amino acid vulnerabilities in cancer

5.35 – 6.05 pm COFFEE BREAK

6.05 – 6.50 pm RICK MORIMOTO (Northwestern University, Evanston, US)

Regulation of the heat shock response and proteostasis networks

Chair MATTHIAS MAYER (ZMBH Heidelberg University, Heidelberg, DE)

6.50 – 7.20 pm POSTER POWER SHOW

15x 2 min short talks of selected poster presenters

7.20 – ∼9.30 pm DINNER & POSTER SESSION

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Day 2 (Tuesday, October 23th)

Session II Epigenetics and Environment

Chair GISLENE PEREIRA (COS, DKFZ, ZMBH Heidelberg University, Heidelberg, DE)

9.00 – 9.30 am DON CLEVELAND (University of California, La Jolla, US) Genome instability in cancer: centromeres, micronuclei and

chromothripsis

9.30 – 10.00 am SYLVIA ERHARDT (ZMBH Heidelberg University, Heidelberg, DE) Centromeric chromatin regulation: a balancing act to maintain

genome stability

10.00 – 10.15 am ANNA BABOUR (Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, FR)

mRNP quality control at chromatin: a novel role for the chromatin remodeler ISW1

10.15 – 10.45 am RITWICK SAWARKAR (MPI of Immunobiology and Epigenetics Freiburg, DE)

Chromatin response to environmental stress

10.45 – 11.15 am COFFEE BREAK

Chair FRAUKE MELCHIOR (ZMBH Heidelberg University, Heidelberg, DE)

11.15 – 11.45 am GEORGIOS KARRAS (University of Texas, Houston, US) Fantastic Protein Folding Mutants and Where to Find Them

11.45 – 12.00 pm MOHAMED EL-BROLOSY (MPI for Heart and Lung Research, Bad Nauheim, DE)

Genetic compensation is triggered by mutant mRNA degradation 12.00 – 12.30 pm OLIVIA CASANUEVA (Babraham Institute, Cambridge, UK) Inter-individual variability in neuronal stress drives phenotypic

heterogeneity in isogenic worms

12.30 – 1.00 pm JUDITH ZAUGG (The European Molecular Biology Laboratory (EMBL), Heidelberg, DE)

From epigenetic variation across individuals to disease mechanisms

1.00 – 3.00 pm LUNCH BREAK

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Chair RÜDIGER HELL (COS Heidelberg University, Heidelberg, DE) 3.00 – 3.30 pm OLIVER RANDO (University of Massachusetts, Worcester, US) Paternal environmental effects in mammals

3.30 – 4.00 pm ISABEL BÄURLE (University of Potsdam, Potsdam, DE) How do plants remember a stressful day– a role for epigenetics?

4.00 – 4.30 pm ANJA GROTH (University of Copenhagen, Copenhagen, DK) Chromatin replication and epigenome Maintenance

4.30 – 4.45 pm ORIANA MARQUES (University Hospital Heidelberg, DE) Ferroportin regulation in acute inflammatory stress: is there a role

for NF-кB?

4.45 – 5.15 pm COFFEE BREAK

Session III From Protein Aggregation to Cellular Dysfunction and Death

Chair AURELIO TELEMAN (DKFZ, Heidelberg, DE)

5.15 – 5.45 pm TIAGO OUTEIRO (Göttingen University, Göttingen, DE) From protein misfolding to cellular pathologies: the molecular

basis of neurodegeneration

5.45 – 6.15 pm CARMEN NUSSBAUM (ZMBH Heidelberg University, DKFZ, Heidelberg, DE) Reducing insulin signaling protects against non-cell autonomous lysosomal rupture caused by α-synuclein spreading

6.15 – 6.30 pm RUBEN FERNANDEZ-BUSNADIEGO (MPI for Biochemistry, Martinsried, DE)

Structural insights into proteasome dysfunction in ALS/FTD

6.30 – 6.45 pm ANNE WENTINK (ZMBH Heidelberg University, DKFZ, Heidelberg, DE)

Mechanism of α-synuclein amyloid fibril disaggregation by the human Hsc70 chaperone machinery

8.00 pm SPECIAL EVENT: DINNER RECEPTION AT THE ROSSINI RESTAURANT*

*For speakers and SFB1036 members