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Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme.

ABSTRACT: The kidney develops through reciprocal interactions between two precursor tissues: the metanephric mesenchyme and the ureteric bud. We previously demonstrated that the zinc finger protein Sall1 is essential for ureteric bud attraction toward the mesenchyme. Here, we show that Kif26b, a kinesin family gene, is a downstream target of Sall1 and that disruption of this gene causes kidney agenesis because of impaired ureteric bud attraction. In the Kif26b-null metanephros, compact adhesion between mesenchymal cells adjacent to the ureteric buds and the polarized distribution of integrin alpha8 were impaired, resulting in failed maintenance of Gdnf, a critical ureteric bud attractant. Overexpression of Kif26b in vitro caused increased cell adhesion through interactions with nonmuscle myosin. Thus, Kif26b is essential for kidney development because it regulates the adhesion of mesenchymal cells in contact with ureteric buds.

SUBMITTER: Uchiyama Y

PROVIDER: S-EPMC2889100 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature

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Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme.

Uchiyama Yukako Y Sakaguchi Masaji M Terabayashi Takeshi T Inenaga Toshiaki T Inoue Shuji S Kobayashi Chiyoko C Oshima Naoko N Kiyonari Hiroshi H Nakagata Naomi N Sato Yuya Y Sekiguchi Kiyotoshi K Miki Hiroaki H Araki Eiichi E Fujimura Sayoko S Tanaka Satomi S SS Nishinakamura Ryuichi R

Proceedings of the National Academy of Sciences of the United States of America 20100503 20

The kidney develops through reciprocal interactions between two precursor tissues: the metanephric mesenchyme and the ureteric bud. We previously demonstrated that the zinc finger protein Sall1 is essential for ureteric bud attraction toward the mesenchyme. Here, we show that Kif26b, a kinesin family gene, is a downstream target of Sall1 and that disruption of this gene causes kidney agenesis because of impaired ureteric bud attraction. In the Kif26b-null metanephros, compact adhesion between me ...[more]

PMID: 20439720

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Project description:The developing pancreatic epithelium gives rise to all endocrine and exocrine cells of the mature organ. During organogenesis, the epithelial cells receive essential signals from the overlying mesenchyme. Previous studies, focusing on ex vivo tissue explants or complete knockout mice, have identified an important role for the mesenchyme in regulating the expansion of progenitor cells in the early pancreas epithelium. However, due to the lack of genetic tools directing expression specifically to the mesenchyme, the potential roles of this supporting tissue in vivo, especially in guiding later stages of pancreas organogenesis, have not been elucidated. We employed transgenic tools and fetal surgical techniques to ablate mesenchyme via Cre-mediated mesenchymal expression of Diphtheria Toxin (DT) at the onset of pancreas formation, and at later developmental stages via in utero injection of DT into transgenic mice expressing the Diphtheria Toxin receptor (DTR) in this tissue. Our results demonstrate that mesenchymal cells regulate pancreatic growth and branching at both early and late developmental stages by supporting proliferation of precursors and differentiated cells, respectively. Interestingly, while cell differentiation was not affected, the expansion of both the endocrine and exocrine compartments was equally impaired. To further elucidate signals required for mesenchymal cell function, we eliminated ?-catenin signaling and determined that it is a critical pathway in regulating mesenchyme survival and growth. Our study presents the first in vivo evidence that the embryonic mesenchyme provides critical signals to the epithelium throughout pancreas organogenesis. The findings are novel and relevant as they indicate a critical role for the mesenchyme during late expansion of endocrine and exocrine compartments. In addition, our results provide a molecular mechanism for mesenchymal expansion and survival by identifying ?-catenin signaling as an essential mediator of this process. These results have implications for developing strategies to expand pancreas progenitors and ?-cells for clinical transplantation.

Dataset Information

Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme.

Publications

Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme.

Similar Datasets

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