H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration.

H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Research Abstract Details 

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H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Abstract Text:

Dany S Adams,Alessio Masi,Michael Levin,

In many systems, ion flows and long-term endogenous voltage gradients regulate patterning events, but molecular details remain mysterious. To establish a mechanistic link between biophysical events and regeneration, we investigated the role of ion transport during Xenopus tail regeneration. We show that activity of the V-ATPase H(+) pump is required for regeneration but not wound healing or tail development. The V-ATPase is specifically upregulated in existing wound cells by 6 hours post-amputation. Pharmacological or molecular genetic loss of V-ATPase function and the consequent strong depolarization abrogates regeneration without inducing apoptosis. Uncut tails are normally mostly polarized, with discrete populations of depolarized cells throughout. After amputation, the normal regeneration bud is depolarized, but by 24 hours post-amputation becomes rapidly repolarized by the activity of the V-ATPase, and an island of depolarized cells appears just anterior to the regeneration bud. Tail buds in a non-regenerative ;refractory' state instead remain highly depolarized relative to uncut or regenerating tails. Depolarization caused by V-ATPase loss-of-function results in a drastic reduction of cell proliferation in the bud, a profound mispatterning of neural components, and a failure to regenerate. Crucially, induction of H(+) flux is sufficient to rescue axonal patterning and tail outgrowth in otherwise non-regenerative conditions. These data provide the first detailed mechanistic synthesis of bioelectrical, molecular and cell-biological events underlying the regeneration of a complex vertebrate structure that includes spinal cord, and suggest a model of the biophysical and molecular steps underlying tail regeneration. Control of H(+) flows represents a very important new modality that, together with traditional biochemical approaches, may eventually allow augmentation of regeneration for therapeutic applications.

H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Publishing Authors By Initials

DS Adams,A Masi,M Levin,

For similar animals: chordata: vertebrates: amphibia: anura: pipidae: xenopus research abstracts see: animals: chordata: vertebrates: amphibia: anura: pipidae: xenopus research

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H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Development (Cambridge, England)

VOLUME: 134

Page Numbers: 1323-35

Journal Abbreviation: Development

ISSN: 0950-1991

DAY: 28

MONTH: 02

YEAR: 2007

H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8701744

H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Keywords Mesh Terms:

KEYWORDS: Xenopus

MESH TERMS: physiology

Chemical & Substance for Abstract: H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration. Information

Substance Name: Vacuolar Proton-Translocating ATPases

Registry Number: EC 3.6.1.-

Grant and Affiliation Information for H+ pump-dependent changes in membrane voltage are an early mechanism necessary and sufficient to induce Xenopus tail regeneration.

AFFILIATION: Center for Regenerative and Developmental Biology, Forsyth Institute, and Developmental Biology Department, Harvard School of Dental Medicine, 140 The Fenway, Boston, MA 02115, USA.

Country: England

AGENCY: United States NCRR

GRANT: P41 RR 001395

ACRONYM: RR

MEDLINETA: Development

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