Saltatory control of isometric growth in the zebrafish caudal fin is disrupted in long fin and rapunzel mutants

被引:46
作者
Goldsmith, MI [1 ]
Fisher, S
Waterman, R
Johnson, SL
机构
[1] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA
[3] Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD 21287 USA
关键词
zebrafish; Danio rerio; fin; growth; saltatory growth; overgrowth; cell proliferation; isometric growth; longfin; rapunzel;
D O I
10.1016/S0012-1606(03)00186-6
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Zebrafish fins grow by sequentially adding new segments of bone to the distal end of each fin ray. In wild type zebrafish, segment addition is regulated such that an isometric relationship is maintained between fin length and body length over the lifespan of the growing fish. Using a novel, surrogate marker for fin growth in conjunction with cell proliferation assays, we demonstrate here that segment addition is not continuous, but rather proceeds by saltation. Saltation is a fundamental growth mechanism shared by disparate vertebrates, including humans. We further demonstrate that segment addition proceeds in conjunction with cyclic bursts of cell proliferation in the distal fin ray mesenchyme. In contrast, cells in the distal fin epidermis proliferate at a constant rate throughout the fin ray growth cycle. Finally, we show that two separate fin overgrowth mutants, long fin and rapunzel, bypass the stasis phase of the fin ray growth cycle to develop asymmetrical and symmetrical fin overgrowth, respectively. (C) 2003 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:303 / 317
页数:15
相关论文
共 58 条
  • [1] [Anonymous], 1998, The developing human: Clinically oriented embryology
  • [2] Whole-genome shotgun assembly and analysis of the genome of Fugu rubripes
    Aparicio, S
    Chapman, J
    Stupka, E
    Putnam, N
    Chia, J
    Dehal, P
    Christoffels, A
    Rash, S
    Hoon, S
    Smit, A
    Gelpke, MDS
    Roach, J
    Oh, T
    Ho, IY
    Wong, M
    Detter, C
    Verhoef, F
    Predki, P
    Tay, A
    Lucas, S
    Richardson, P
    Smith, SF
    Clark, MS
    Edwards, YJK
    Doggett, N
    Zharkikh, A
    Tavtigian, SV
    Pruss, D
    Barnstead, M
    Evans, C
    Baden, H
    Powell, J
    Glusman, G
    Rowen, L
    Hood, L
    Tan, YH
    Elgar, G
    Hawkins, T
    Venkatesh, B
    Rokhsar, D
    Brenner, S
    [J]. SCIENCE, 2002, 297 (5585) : 1301 - 1310
  • [3] BECKWITH J B, 1969, Birth Defects Original Article Series, V5, P188
  • [4] Bernstein I M, 1996, Obstet Gynecol Surv, V51, P213, DOI 10.1097/00006254-199604000-00005
  • [5] An oligonucleotide fingerprint normalized and expressed sequence tag characterized zebrafish cDNA library
    Clark, MD
    Hennig, S
    Herwig, R
    Clifton, SW
    Marra, MA
    Lehrach, H
    Johnson, SL
    [J]. GENOME RESEARCH, 2001, 11 (09) : 1594 - 1602
  • [6] Cohen M M Jr, 1999, Adv Pediatr, V46, P441
  • [7] Skeletal overgrowth and deafness in mice lacking fibroblast growth factor receptor 3
    Colvin, JS
    Bohne, BA
    Harding, GW
    McEwen, DG
    Ornitz, DM
    [J]. NATURE GENETICS, 1996, 12 (04) : 390 - 397
  • [8] Size control in animal development
    Conlon, I
    Raff, M
    [J]. CELL, 1999, 96 (02) : 235 - 244
  • [9] Favus M.J., 1999, PRIMER METABOLIC BON
  • [10] Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway
    Goberdhan, DCI
    Paricio, N
    Goodman, EC
    Mlodzik, M
    Wilson, C
    [J]. GENES & DEVELOPMENT, 1999, 13 (24) : 3244 - 3258