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Oxygen as a limiting ecological variable for invertebrate tissue maintenance

ABSTRACT: Ambient oxygen shapes tissue physiology, yet whether elevated oxygen directly perturbs stem cell fate and regeneration in invertebrates remains unclear. Here we test how chronic oxygen exposure influences intestinal stem cell (ISC) behaviour, epithelial homeostasis, and survival in Drosophila melanogaster, an organism lacking vertebrate-style stemness buffering via HIF-2a-driven pseudohypoxia. Adult flies were maintained under an atmosphere with moderate hypoxia (10% oxygen), normoxia (20% oxygen), and hyperoxia (40% oxygen) and assessed by lifespan analysis, midgut immunostaining, and intestinal transcriptomics. Hyperoxia markedly shortened lifespan, revealing high oxygen as a strong constraint on adult Drosophila viability. In the midgut, elevated O2 increased apoptosis and altered lineage outputs, with evidence of impaired fate segregation (mixed stem/differentiation marker expression) and a shift toward enteroendocrine differentiation. Consistent with these cellular phenotypes, transcriptomic profiling of the intestines at the onset of elevated mortality indicated enrichment of inflammatory signalling that compromised epithelial homeostasis. Together, our data support a model in which hyperoxia induces a ‘non-productive regenerative state’, where ISCs persist but their fate regulation and progeny survival are disrupted, leading to epithelial degeneration and reduced organismal viability. These findings position ambient oxygen as a key environmental variable that can destabilize stem cell-driven renewal in invertebrate tissues and motivate comparative studies on how oxygen-sensing strategies shape regenerative capacity across animal lineages.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE324332 | GEO | 2026/03/09

REPOSITORIES: GEO

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Project description:Adipose tissue is a plentiful and easily accessible source of mesenchymal stem cells that have been shown to be multi potent and possibly have immuno suppressive capacity(Zuk, Zhu et al. 2002; McIntosh, Zvonic et al. 2006; Prichard, Reichert et al. 2008). Several studies have identified hypoxia and the molecular effector of reduced oxygen tension, HIF1Î± to be essential in the differentiation processes, stem cell proliferation and survival as well as in maintenance of stem cell characteristics (Lennon, Edmison et al. 2001; Goda, Ryan et al. 2003; Wang, Fermor et al. 2005; Lin, Lee et al. 2006; Malladi, Xu et al. 2007; Ohnishi, Yasuda et al. 2007). The fact that oxygen has a central role in cell development and metabolism makes the regulation of oxygen tension a valuable tool in the attempt of exploiting stem cells to their full potential. In the current study we investigate the transcriptional changes caused by two weeks of monolayer hypoxic expansion of human adipose tissue derived stem cells (ASCs). Application of the XVivo hypoxic workstation (BioSpherix, Redfield, NY) made it possible to conduct the expansion of six ASC lines at four different hypoxic conditions in parallel covering the range from mild (15% oxygen) to full hypoxic (1% oxygen) conditions. In this comprehensive investigation the Illumina bead microarray platform was employed to give a profound and new insight in the molecular changes effectuated by hypoxic expansion. The findings of this study demonstrate the significance of biologic variation in the transcriptional response to mild hypoxic expansion and display evidence that full hypoxic growth conditions at 1% oxygen tension selects for a more prolific cell population of reduced chondrogenic potential. Keywords: hypoxia response To investigate the transcriptional response to hypoxia, adipose tissue derived stem cells (ASCs) from six female individuals were cultured for 14 days at different oxygen tensions (ambient, 15%, 10%, 5% and 1%). Gene expression levels at each oxygen tension were compared to ambient conditions (Ambient oxygen tension) using Illumina Human-6 v2.0 microarrays.

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Oxygen as a limiting ecological variable for invertebrate tissue maintenance

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