Mobilisation of jerboa kidney gene networks during dehydration and opportunistic rehydration
Benjamin T. Gillard,
Nabil Amor,
Fernando Alvira Iraizoz,
Audrys G. Pauža,
Colin Campbell,
Michael P. Greenwood,
Abdulaziz N. Alagaili,
David Murphy
Affiliations
Benjamin T. Gillard
Molecular Neuroendocrinology Research Group, Bristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, England
Nabil Amor
LR18ES05, Laboratory of Biodiversity, Parasitology and Ecology of Aquatic Ecosystems, Department of Biology - Faculty of Sciences of Tunis, University of Tunis El Manar, Tunisia
Fernando Alvira Iraizoz
Molecular Neuroendocrinology Research Group, Bristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, England
Audrys G. Pauža
Molecular Neuroendocrinology Research Group, Bristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, England
Colin Campbell
Department of Engineering Mathematics, Ada Lovelace Building, University of Bristol, Bristol, England
Michael P. Greenwood
Molecular Neuroendocrinology Research Group, Bristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, England
Abdulaziz N. Alagaili
Department of Zoology, King Saud University, Riyadh, Kingdom of Saudi Arabia
David Murphy
Molecular Neuroendocrinology Research Group, Bristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, England; Corresponding author
Summary: Desert animals have evolved systems that enable them to thrive under dry conditions. Focusing on the kidney, we have investigated the transcriptomic adaptations that enable a desert rodent, the Lesser Egyptian Jerboa (Jaculus jaculus), to withstand water deprivation and opportunistic rehydration. Analysis of the whole kidney transcriptome showed many differentially expressed genes in the Jerboa kidney, 6.4% of genes following dehydration and an even greater number (36.2%) following rehydration compared to control. Genes correlated with the rehydration condition included many ribosomal protein coding genes suggesting a concerted effort to accelerate protein synthesis when water is made available. We identify an increase in TGF-beta signaling antagonists in dehydration (e.g., GREM2). We also describe expression of multiple aquaporin and solute carrier transporters mapped to specific nephron segments. The desert adapted renal transcriptome presented here is a valuable resource to expand our understanding of osmoregulation beyond that derived from model organisms.
