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Originally published as MBC in Press, 10.1091/mbc.E02-07-0438 on October 16, 2002
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Vol. 13, Issue 12, 4111-4113, December 2002

ESSAY
Mammalian Septins Nomenclature

Ian G. Macara,*dagger Richard Baldarelli,Dagger Christine M. Field,§ Michael Glotzer,|| Yasuhide Hayashi, Shu-Chan Hsu,# Mary B. Kennedy,@ Makoto Kinoshita,§ Mark Longtine,** Claudia Low,dagger dagger Lois J. Maltais,Dagger Louise McKenzie,Dagger Timothy J. Mitchison,§ Toru Nishikawa,Dagger Dagger Makoto Noda,§§ Elizabeth M. Petty,|||| Mark Peifer,¶¶ John R. Pringle,¶¶ Phillip J. Robinson,## Dagmar Roth,@@ S.E. Hilary Russell,*** Heidi Stuhlmann,dagger dagger dagger Manami Tanaka,Dagger Dagger Dagger Tomoo Tanaka,§§§ William S. Trimble,|||||| Jerry Ware,¶¶¶ Nancy J. Zeleznik-Le,### and Barbara Zieger@@@

 *Center for Cell Signaling, University of Virginia School of Medicine, Charlottesville, Virginia 22908;  Dagger Mouse Genome Informatics, Jackson Laboratories, Bar Harbor, Maine 04609;  §Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115;  ||Research Institute of Molecular Pathology, A-1030 Vienna, Austria;  Department of Pediatrics, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan;  #Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854;  @Division of Biology, California Institute of Technology, Pasadena, California 91125;  **Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, Oklahoma 74078;  dagger dagger Department of Biochemistry, University of Virginia School of Medicine, Charlottesville, Virginia 22908;  Dagger Dagger Section of Psychiatry and Behavioral Sciences, Tokyo Medical and Dental University Graduate School, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan;  §§Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan;  ||||Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109;  ¶¶Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599;  ##Cell Signaling Unit, Children's Medical Research Institute, Wentworthville 2145, New South Wales, Australia;  @@Max-Planck-Institute for Brain Research, Department of Neurochemistry, Frankfurt, and Covidence GmbH, Philipp-Helfmann-Strasse 18, D-65760 Eschborn, Germany;  ***Department of Oncology, Queen's University of Belfast, Belfast BT9 7AB, United Kingdom;  dagger dagger dagger Department of Biochemistry and Molecular Biology, Mount Sinai School of Medicine, New York, New York 10029;  Dagger Dagger Dagger National Institute of Advanced Industrial Science and Technology, Bldg. Tsukuba Central 6, Higashi, Tsukuba Science City, Ibaraki 305-8566, Japan;  §§§Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan;  ||||||Program in Cell Biology, Hospital for Sick Children, University of Toronto, Toronto, Ontario M5G 1X8, Canada;  ¶¶¶The Scripps Research Institute, La Jolla, California 92037;  ###Cardinal Bernardin Cancer Center and Department of Medicine, Loyola University Medical, Center, Maywood, Illinois 60153; and  @@@Department of Pediatrics and Adolescent Medicine, Children's Hospital, University of Freiburg, D-79106 Freiburg, Germany

Submitted July 29, 2002; Revised September 11, 2002; Accepted September 24, 2002
Monitoring Editor: Suzanne R. Pfeffer

    ABSTRACT
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ABSTRACT
ARTICLE

There are 10 known mammalian septin genes, some of which produce multiple splice variants. The current nomenclature for the genes and gene products is very confusing, with several different names having been given to the same gene product and distinct names given to splice variants of the same gene. Moreover, some names are based on those of yeast or Drosophila septins that are not the closest homologues. Therefore, we suggest that the mammalian septin field adopt a common nomenclature system, based on that adopted by the Mouse Genomic Nomenclature Committee and accepted by the Human Genome Organization Gene Nomenclature Committee. The human and mouse septin genes will be named SEPT1-SEPT10 and Sept1-Sept10, respectively. Splice variants will be designated by an underscore followed by a lowercase "v" and a number, e.g., SEPT4_v1.

    ARTICLE
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ARTICLE

The septins are a family of proteins that were first discovered in the yeast Saccharomyces cerevisiae by analysis of mutants defective in cytokinesis and bud morphogenesis. It is now clear that they are widespread and probably ubiquitous in the fungi and animals, although apparently not in plants. Most if not all septins seem to bind and hydrolyze GTP and to participate in filament formation in vitro and probably in vivo. In addition to their widespread involvement in cytokinesis, the septins seem also to be involved in vesicle trafficking and other aspects of cell surface organization, and they may have other functions as well. For various trivial historical reasons, the current nomenclature for the mammalian septins is particularly chaotic and confusing. With the field still young but attracting increasing interest, there seems to be great value in rationalizing and simplifying the septin nomenclature at this time.

In accordance with the Mouse Genomic Nomenclature Committee nomenclature, the mouse genes will be named Sept1-Sept10, and the corresponding protein products will be SEPT1-SEPT10. Although these numbers do not correspond to the genetic distances between the septins (Figure 1), they do provide an unambiguous and consistent naming system. The Human Genome Organization Gene Nomenclature Committee-approved symbols will be SEPT1-SEPT10 for the genes, and the corresponding gene products will be SEPT1-SEPT10. Although there are still too few sequences available to be certain, it seems likely that most or all septins of other vertebrates will prove to have unambiguous orthologues among the mammalian septins, in which case it would be desirable to name them by using the same system. For example, several fragments of septin genes from frog and zebrafish are available in GenBank as expressed sequence tags (ESTs), and these encode peptides that are highly related to particular mammalian septins. Therefore, we suggest that where possible other vertebrate septins be named using the same system as used for the mammalian proteins. Usually, the species being described would be obvious from the context, but it could also be indicated by adding, as a prefix, an abbreviation of the Latin binomial for the species (e.g., Xl for Xenopus laevis). For example, the frog septin A (GenBank no. AF212298), which is 89% similar in sequence to human SEPT2 but only 61% similar to the next most closely related human septin, would now be named Xl SEPT2, or just SEPT2. (However, the prefix would not be a part of the official gene symbol.) At the same time, comparison of the yeast, Caenorhabditis elegans and Drosophila septins to the mammalian septins (Adam, Peifer, and Pringle, unpublished data) shows that the relationships are sufficiently complicated that the mammalian nomenclature scheme could not reasonably be applied to nonvertebrate septins.


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Figure 1.   Unrooted phylogenetic tree of human septins. This consensus tree was generated using the Protpars program in the Phylip package. Each of the 1000 bootstrapped replicate data sets generated was analyzed 20 times, with the sequence input order randomized each time. The branch values (percentage) refer to the frequency with which a given branching pattern was produced. Strong support for any particular branch shown in the figure is indicated by values >90%, and moderate-to-weak support is indicated by values between 60 and 90%. Values <60% indicate no support for the given branching pattern. Segment lengths do not correspond to relatedness.

The proposed symbols are reconciled with the previously used aliases for the mouse and human members of the septin family in Table 1. This table also provides selected GenBank accession numbers for the mouse and human septins, the N- and C-terminal sequences of the longest known variants (so as to provide an unambiguous means of identification), and the human chromosome loci.

                              
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Table 1.  Proposed nomenclature for mammalian septins

Note that some septins currently have a multitude of distinct aliases (e.g., SEPT9 names include Sint1, Sep9, E-septin, SLP-a, MSF, SepD1, and Ov/Br septin), and SEPT6 has been named both Septin 6 and Sept2, which engenders considerable confusion in the literature and in database searches. Additionally, some vertebrate septins (e.g., Cdc10 or Pnutl) have been named after Saccharomyces cerevisiae or Drosophila septins that are not true orthologues (or even the closest homologues). Finally, at least four septin genes produce multiple splice variants, and these have also sometimes been given completely different names [e.g., SEPT4 splice variants include hCDCrel-2a, hCDCrel-2b, Bradeion-alpha and -B, ARTS, MART, and Pnutl2(variants 1-4)]. To make the genetic origin of these variants clear, we propose using the system adopted by the Mouse and Human Genome Nomenclature Committees. In this system, splice variants are distinguished by an underscore followed by a lowercase "v" and a number, as listed in Table 1, e.g., the mouse G-septin alpha  would be named SEPT3_v1. Finally, we propose that if new, distinct septin genes are discovered, they and their products be given a new number in the sequence (e.g., SEPT11).

    FOOTNOTES

dagger Corresponding author. E-mail address: igm9c{at}virginia.edu.

Article published online ahead of print. Mol. Biol. Cell 10.1091/mbc.E02-07-0438. Article and publication date are at www.molbiolcell.org/cgi/doi/10.1091/mbc.E02-07-0438.


Molecular Biology of the Cell
Vol. 13, 4111-4113, December 2002
Copyright © 2002 by The American Society for Cell Biology



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