pbx is required for pole and eye regeneration in planarians

Development. 2013 Feb;140(4):719-29. doi: 10.1242/dev.083741. Epub 2013 Jan 14.

Abstract

Planarian regeneration involves regionalized gene expression that specifies the body plan. After amputation, planarians are capable of regenerating new anterior and posterior poles, as well as tissues polarized along the anterior-posterior, dorsal-ventral and medial-lateral axes. Wnt and several Hox genes are expressed at the posterior pole, whereas Wnt inhibitory genes, Fgf inhibitory genes, and prep, which encodes a TALE-family homeodomain protein, are expressed at the anterior pole. We found that Smed-pbx (pbx for short), which encodes a second planarian TALE-family homeodomain transcription factor, is required for restored expression of these genes at anterior and posterior poles during regeneration. Moreover, pbx(RNAi) animals gradually lose pole gene expression during homeostasis. By contrast, pbx was not required for initial anterior-posterior polarized responses to wounds, indicating that pbx is required after wound responses for development and maintenance of poles during regeneration and homeostatic tissue turnover. Independently of the requirement for pbx in pole regeneration, pbx is required for eye precursor formation and, consequently, eye regeneration and eye replacement in homeostasis. Together, these data indicate that pbx promotes pole formation of body axes and formation of regenerative progenitors for eyes.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Body Patterning / physiology*
  • Gene Expression Regulation, Developmental / physiology*
  • Homeodomain Proteins / metabolism*
  • Image Processing, Computer-Assisted
  • In Situ Hybridization
  • In Situ Hybridization, Fluorescence
  • Microscopy, Fluorescence
  • Ocular Physiological Phenomena*
  • Planarians / physiology*
  • RNA Interference
  • Regeneration / physiology*
  • Transcription Factors / metabolism*

Substances

  • Homeodomain Proteins
  • Transcription Factors