Subarea 2: Regeneration and Homeostasis of Organs in Aging

The main goal of Subarea 2 is to identify cellular and molecular pathways used to ensure effective organ maintenance and repair, and to unravel the mechanisms of their deterioration during aging. While stem cells are important for organ homeostasis, this Subarea does not per se directly addresses stem cell aging but rather focusses on the following focus areas:

Drifts in developmental pathways limiting organ maintenance in aging,
Immune aging and inflammation, and
Systemic and micro-milieu regulators of organ maintenance, regeneration, and disease development.

Research focus of Subarea 2

Organ maintenance is regulated by local and systemic factors, which are subject to aging-associated changes. Research of Subarea 2 focuses on the following research areas: a) Genetic and epigenetic modulation of developmental pathways has been shown to contribute to progressive aging and disease. It is critical to delineate mechanisms and consequences of aging-associated drifts to better understand organ maintenance during aging. b) Immunoaging and chronic inflammation elicits negative effects through reduced immune surveillance and aberrant organ repair and maintenance; all of which contributes to the evolution of organ pathologies and diseases during organismal aging. c) Furthermore, aging-associated alterations in systemic and extracellular factors derived from metabolic changes, microbiota alterations, chronic inflammation, senescent, or damaged cells might impinge on disease development and tumor initiation.

Publications

(since 2016)

2017

Developmental stage-dependent regulation of spine formation by calcium-calmodulin-dependent protein kinase IIα and Rap1.
Koeberle SC, Tanaka S, Kuriu T, Iwasaki H, Koeberle A, Schulz A, Helbing DL, Yamagata Y, Morrison H, Okabe S
Sci Rep 2017, 7(1), 13409
Ustilago maydis effectors and their impact on virulence.
Lanver D, Tollot M, Schweizer G, Lo Presti L, Reissmann S, Ma LS, Schuster M, Tanaka S, Liang L, Ludwig N, Kahmann R
Nat Rev Microbiol 2017, 15(7), 409-21
Spindle Misorientation of Cerebral and Cerebellar Progenitors Is a Mechanistic Cause of Megalencephaly.
Li H, Kroll T, Moll J, Frappart L, Herrlich P, Heuer H, Ploubidou A
Stem Cell Reports 2017, 9(4), 1071-80
Regulators of cell crosstalk crucial for bone mass
Liu P
Dissertation 2017, Ulm, Germany
Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis.
Liu P, Lee S, Knoll J, Rauch A, Ostermay S, Luther J, Malkusch N, Lerner UH, Zaiss MM, Neven M, Wittig R, Rauner M, David JP, Bertolino P, Zhang CX, Tuckermann JP
Cell Death Differ 2017, 24(4), 672-82
Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP activity.
Mindos T, Dun XP, North K, Doddrell RDS, Schulz A, Edwards P, Russell J, Gray B, Roberts SL, Shivane A, Mortimer G, Pirie M, Zhang N, Pan D, Morrison H, Parkinson DB
J Cell Biol 2017, 216(2), 495-510
Vitamin A regulates Akt signaling through the phospholipid fatty acid composition.
Pein* H, Koeberle* SC, Voelkel M, Schneider F, Rossi A, Thürmer M, Loeser K, Sautebin L, Morrison H, Werz O, Koeberle A
FASEB J 2017, 31(10), 4566-77 * equal contribution
Central immune tolerance depends on crosstalk between the classical and alternative NF-κB pathways in medullary thymic epithelial cells.
Riemann M, Andreas N, Fedoseeva M, Meier E, Weih D, Freytag H, Schmidt-Ullrich R, Klein U, Wang ZQ, Weih F
J Autoimmun 2017, 81, 56-67
Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development.
Stopp S, Gründl M, Fackler M, Malkmus J, Leone M, Naumann R, Frantz S, Wolf E, von Eyss B, Engel FB, Gaubatz S
Proc Natl Acad Sci U S A 2017, 114(30), 8029-34 published during change of institution
RHEB1 insufficiency in aged male mice is associated with stress-induced seizures.
Tian Q, Gromov P, Clement JH, Wang Y, Riemann M, Weih F, Sun XX, Dai MS, Fedorov LM
Geroscience 2017, 39(5-6), 557-70