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Background  Wnt11 is a member of the Wnt family of secreted signals controlling the early steps in ureteric bud (UB) branching. Due to the reported lethality of  Wnt11  knockout embryos  in utero , its role in later mammalian kidney organogenesis remains open. The presence of Wnt11 in the emerging tubular system suggests that it may have certain roles later in the development of the epithelial ductal system.    Results  The  Wnt11  knockout allele was backcrossed with the  C57Bl6  strain for several generations to address possible differences in penetrance of the kidney phenotypes. Strikingly, around one third of the null mice with this inbred background survived to the postnatal stages. Many of them also reached adulthood, but urine and plasma analyses pointed out to compromised kidney function. Consistent with these data the tubules of the  C57Bl6 Wnt11   −/−   mice appeared to be enlarged, and the optical projection tomography indicated changes in tubular convolution. Moreover, the  C57Bl6 Wnt11   −/−   mice developed secondary glomerular cysts not observed in the controls. The failure of  Wnt11  signaling reduced the expression of several genes implicated in kidney development, such as  Wnt9b ,  Six2 ,  Foxd1  and  Hox10 . Also  Dvl2 , an important PCP pathway component, was downregulated by more than 90 % due to  Wnt11  deficiency in both the E16.5 and NB kidneys. Since all these genes take part in the control of UB, nephron and stromal progenitor cell differentiation, their disrupted expression may contribute to the observed anomalies in the kidney tubular system caused by  Wnt11  deficiency.    Conclusions  The Wnt11 signal has roles at the later stages of kidney development, namely in coordinating the development of the tubular system. The  C57Bl6 Wnt11   −/−   mouse generated here provides a model for studying the mechanisms behind tubular anomalies and glomerular cyst formation.    Electronic supplementary material  The online version of this article (doi:10.1186/s12861-016-0131-z) contains supplementary material, which is available to authorized users.

Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis