Defects in nephrogenesis result in an expansion of the <i>Foxd1</i>+ stromal progenitor population.

ABSTRACT: Reciprocal signaling interactions coordinate multiple aspects of kidney development. While signals from the stroma have been shown to regulate nephron progenitor cell (NPC) differentiation, much less is known about regulation of the stromal progenitor population. Here, we demonstrate that disruption of the NPC lineage via loss of Wt1 (i.e., Six2cre;Wt1 ^c/c ) results in an expansion of Foxd1+ stromal progenitor cells. Analyses of the developing stroma in two additional models, including Wnt4-null mutants (which fail to form nephron structures similar to Six2cre;Wt1 ^c/c kidneys) and NPC ablation via diphtheria toxin (i.e., Six2cre;RosaDTA ^c/+ ), both phenocopy Six2cre;Wt1 ^c/c

SUBMITTER: Michalopulos MG 

PROVIDER: S-EPMC11844377 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature