Publication Date:
2005-12-24
Description:
Epimorphic regeneration requires the presence or creation of pluripotent cells capable of reproducing lost organs. Zebrafish fin regeneration is mediated by the creation of blastema cells. Here, we characterize the devoid of blastema (dob) mutant that fails fin regeneration during initial steps, forms abnormal regeneration epithelium, and does not form blastema. This mutation has no impact on embryonic survival. Dob results from an fgf20a null mutation, Y148S. Fgf20a is expressed during initiation of fin regeneration at the epithelial-mesenchymal boundary and later overlaps with the blastema marker msxb. Thus, fgf20a has a regeneration-specific requirement, initiating fin regeneration, and controlling blastema formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitehead, Geoffrey G -- Makino, Shinji -- Lien, Ching-Ling -- Keating, Mark T -- New York, N.Y. -- Science. 2005 Dec 23;310(5756):1957-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16373575" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Extremities
;
Fibroblast Growth Factors/*physiology
;
Homeodomain Proteins/biosynthesis
;
Male
;
Mesoderm
;
Mutation
;
Regeneration/genetics/*physiology
;
Temperature
;
Wound Healing
;
Zebrafish
;
Zebrafish Proteins/biosynthesis/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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