Common and divergent roles for members of the mouse DCX superfamily

Frédéric M. Coquelle, Talia Levy, Sven Bergmann, Sharon Grayer Wolf, Daniela Bar-El, Tamar Sapir, Yehuda Brody, Irit Orr, Naama Barkai, Gregor Eichele, Orly Reiner

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


The doublecortin-like (DCX) domains serve as protein-interaction platforms. DCX tandem domains appear in the product of the X-linked doublecortin (DCX) gene, in retinitis pigmentosa-1 (RP1), as well as in other gene products. Mutations in the human DCX gene are associated with abnormal neuronal migration, epilepsy, and mental retardation; mutations in RP1 are associated with a form of inherited blindness, while DCDC2 has been associated with dyslectic reading disabilities. Motivated by the possible importance of this gene family, a thorough analysis to detect all family members in the mouse was conducted. The DCX-repeat gene superfamily is composed of eleven paralogs, and we cloned the DCX domains from nine different genes. Our study questioned which functions attributed to the DCX domain, are conserved among the different members. Our results suggest that the proteins with the DCX-domain have conserved and unique roles in microtubule regulation and signal transduction. All the tested proteins stimulated microtubule assembly in vitro. Proteins with tandem repeats stabilized the microtubule cytoskeleton in transfected cells, while those with single repeats localized to actin-rich subcellular structures, or the nucleus. All tested proteins interacted with components of the JNK/MAP-kinase pathway, while only a subset interacted with Neurabin 2, and a nonoverlapping group demonstrated actin association. The sub-specialization of some members due to confined intracellular localization, and protein interactions may explain the success of this superfamily.

Original languageEnglish
Pages (from-to)976-983
Number of pages8
JournalCell Cycle
Issue number9
StatePublished - 1 May 2006
Externally publishedYes

Bibliographical note

Funding Information:
We thank Prof. Shmuel Pietrekovski, and Dr. Arlette Fellous for helpful discussions. The work has been supported in part by the Fritz Thyseen Stifung Foundation, the Israeli Science Foundation (grant no. 270/04), Foundation Jérôme Lejeune, Minerva foundation with funding from the Federal German Ministry for Education and Research, the German-Israeli collaboration grant Gr-1905, the Kekst center, the David and Fela Shapell Family Center for Genetic Disorders Research. O.R. is an Incumbent of the Berstein-Mason professorial chair of Neurochemistry. F.C. was supported by a Post-Doctoral Fellowship from the Association pour la Recherche sur le Cancer (Villejuif, France), and by the Sir Charles Clore Post-Doctoral Fellowship, the Weizmann Institute of Science (Rehovot, Israel).


  • Actin
  • Cytoskeleton
  • Doublecortin
  • Intracellular localization
  • Microtubules
  • Protein family


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