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Interdisciplinary Research

These papers were selected from multiple disciplines from the Faculty of 1000, a Web-based literature awareness tool http://www.facultyof1000.com.A. O'Doherty et al., "An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes," Science, 309:2033–7, Sept. 23, 2005.This is the first study to show that a human chromosome can be introduced into a mouse's germline and transmitted to successive generations. The authors introduced a copy of human chromosome 21. The mice

November 7, 2005

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These papers were selected from multiple disciplines from the Faculty of 1000, a Web-based literature awareness tool http://www.facultyof1000.com.

A. O'Doherty et al., "An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes," Science, 309:2033–7, Sept. 23, 2005.

This is the first study to show that a human chromosome can be introduced into a mouse's germline and transmitted to successive generations. The authors introduced a copy of human chromosome 21. The mice carrying the human chromosome developed cardiac and other morphological abnormalities consistent with Down syndrome. This mouse now provides a potentially very useful model.

Colin StewartNational Cancer Institute, USA

K.Y. Wu et al., "Local translation of RhoA regulates growth cone collapse," Nature, 436:1020–4, Aug. 18, 2005.

This is the first study to show that Semaphorin 3A-dependent signaling triggers local translation of the small GTPase RhoA at the growth cone leading to growth cone collapse, thus linking this pathway to translational control. The effect of Semaphorin 3A, which presumably is mediated through its receptor plexin-A, requires the 3' UTR of RhoA. The involvement of known translational factors localized at the growth cone and their modification as a result of Semaphorin 3A-dependent signaling may further elucidate the molecular basis for growth cone collapse.

Talila VolkWeizmann Institute of Science, Israel

S.L. Harvey et al., "Cdk1-dependent regulation of the mitotic inhibitor wee1," Cell, 122:407–20, Aug. 12, 2005.

Entry into mitosis is controlled by the activity of the Clb-Cdc28 (cyclinB/Cdk1) complex. A comprehensive understanding of how this complex is regulated is needed to understand the transition from G2 to mitosis. Here, the authors show that this Clb-Cdc28 complex is able to directly phosphorylate and activate its own negative regulator, the Swe1 protein kinase, to prevent premature entry into mitosis.

Francesc PosasUniversity Pompeu Fabra, Spain

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