One of the main questions to address during regeneration is to determine how polarity is re-established. By “polarity” meaning that an anterior-facing wound will regenerate the missing anterior structures whereas a posterior-facing wound will regenerate the missing posterior structures. For instance, just think in planarians: if you amputate an animal in 3 pieces: head, trunk and tail, the head piece will regenerate posterior trunk and tail, the trunk piece will regenerate a new head in the anterior-facing wound and a tail in the posterior-facing wound and, finally, the tail piece will regenerate new anterior trunk and head. In recent years it has been shown how the establishment of AP polarity in planarians mainly depends upon the activity of the Wnt/β-catenin pathway. Thus, the silencing of β-catenin leads to the conversion of any posterior blastema into an anterior fate and, conversely, an ectopic activity of β-catenin results in the conversion of any anterior blastema into posterior ones. That means, that multi-headed planarians can be generated after β-catenin knockdown and multi-tailed planarians develop after ectopic expression of β-catenin [Iglesias et al. (2008) Development 135: 1215-1221; Gurley et al. (2008) Science 319: 24-39; Petersen and Reddien (2008) Science 319: 327-330]. Subsequent studies have shown that the Hedgehog (Hh) pathway contributes also to the establishment of AP polarity being required for posterior identity [Rink et al. (2009) Science 326: 1406-1410; Yazawa et al. (2009) PNAS 106: 22329-22334]. Now, two papers in Development from the laboratories of Aziz Aboobaker (http://www.ncbi.nlm.nih.gov/pubmed/23318635) and Peter Reddien (http://www.ncbi.nlm.nih.gov/pubmed/23318641) characterize the function of a planarian pbx gene (a TALE-class homeodomain protein) that is required for the regeneration of both poles, anterior and posterior. Previous works have characterized genes that block either anterior or posterior pole regeneration [Felix and Aboobaker (2010) PLoS Genet 6: e1000915; Hayashi et al. (2011) Development 138: 3679-3688], but pbx represents the first example of a gene required for the regeneration of both poles. In both papers the authors show a significant reduction or complete absence of patterning genes that determine or are specific markers of anterior and posterior poles. Apparently, regeneration polarity would not be completely ablated after pbx silencing but the further development and patterning of those anterior and posterior poles would be in fact blocked. Further experiment should try to determine how pbx could be interacting with different partners at both poles in order to allow the regeneration of specific anterior and posterior tissues and structures.
regeneration in nature
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regeneration in nature 
I agree Chema. It seems that pbx would function a step slightly later than the initial AP polarity signals. At least this is what it appears to be more explicitly suggested in the paper from Peter Reddien’s lab. Therefore, pbx would have a role related to the maintenance of the poles as well as to their further development. What it becomes interesting then is to determine the different partners that pbx can be interacting with in both poles in order to differentiate and pattern the distinct anterior and posterior tissues and structures
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Hi Francesc, both papers seem to agree that pbx is required for pole maintenance, but I’m curious about your opinion on the role of pbx in polarity re-establishment..
As you mentioned, the Reddien paper concludes that pbx is not involved in polarity decisions (since notum and wnt1 are expressed normally at 18 hpa). But notum expression is lost in pbx RNAi animals in the Aboobaker paper, suggesting polarity decisions may be affected… so could it be that phenotype shown in the Reddien paper is just weaker?
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Hi Praer
that is a good observation. But as I understand in the Aboobaker paper they checked notum expression in regenerating tail pieces, whereas in Reddien paper they worked with bipolar regenerating trunks. So, it could be that the effects of pbx(RNAi) could vary along the AP axis. In fact similar differences have been found for other genes involved in AP polarity. Even in the follistatin paper from the Newmark lab you can see in Figure S2 that the effects of the RNAi on brain regeneration appear to be much more severe in tails than in trunks. In any case, it is also interesting to ask ourselves why those defects are stronger in tail pieces.
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Interesting findings. In my opinion, the key question here is how Wnt/betacatenin pathway is related to pbx gene, whether is a direct target or the activation/regulation of pbx comes from a different source. Because, as you pointed out, what was know so far were pathways/genes that had an asymmetric function in the regeneration of the AP polarity (either promoting anterior fates and inhibiting posterior, or the other way around). How is an asymmetric information translated to a gene with a symmetric role (regeneration of both or none)? To me, this seems to indicate that pbx is probably far downstream in the decisions of AP fate, and might be controlling basic processes of morphogenesis, rather than early cell fate. But in any case, another player and another piece to put in this huge and messy jigsaw that is anteroposterior regeneration in adult planarians!!
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