Department of Biotechnology
inStem (Institute for Stem Cell Science and Regenerative Medicine)

S. mediterranea ETS-1 regulates the function of cathepsin-positive cells and the epidermal lineage landscape via basement membrane remodeling.

Publication Type

Research Support, Non-U.S. Gov't

Date of Publication

October 15, 2022

Journal

Journal of cell science

Volume/Issue

135/20

ISSN

1477-9137

Extracellular matrix (ECM) is an important component of stem cell niche. Remodeling of ECM mediated by ECM regulators, such as matrix metalloproteinases (MMPs) plays a vital role in stem cell function. However, the mechanisms that modulate the function of ECM regulators in the stem cell niche are understudied. Here, we explored the role of the transcription factor (TF) ETS-1, which is expressed in the cathepsin-positive cell population, in regulating the expression of the ECM regulator, mt-mmpA, thereby modulating basement membrane thickness. In planarians, the basement membrane around the gut/inner parenchyma is thought to act as a niche for pluripotent stem cells. It has been shown that the early epidermal progenitors migrate outwards from this region and progressively differentiate to maintain the terminal epidermis. Our data shows that thickening of the basement membrane in the absence of ets-1 results in defective migration of stem cell progeny. Furthermore, the absence of ets-1 leads to a defective epidermal progenitor landscape, despite its lack of expression in those cell types. Together, our results demonstrate the active role of ECM remodeling in regulating tissue homeostasis and regeneration in the planarian Schmidtea mediterranea. This article has an associated First Person interview with one of the co-first authors of the paper.

Alternate Journal

J Cell Sci

PubMed ID

36172824

Authors

Vinay Kumar Dubey
Souradeep R Sarkar
Vairavan Lakshmanan
Rimple Dalmeida
Akash Gulyani
Dasaradhi Palakodeti

Keywords

Planarians
Epidermis
Basement Membrane
Mediterranea
Cathepsins
Animals
Matrix Metalloproteinases
Cell Differentiation
Transcription Factors
Humans