The cell cycle and its relation to growth during pattern regulation in wing discs of Drosophila

Role of Jun N-terminal Kinase (JNK) signaling in the wound healing and regeneration of a Drosophila melanogaster wing imaginal disc

“…It is known that after an extensive proliferation during larval development the disc halts its growth; at 0 h APF most of the cells in the wing blade are arrested in G2 (Milan et al 1996), waiting for the hormonal cue to begin an additional round of mitoses and the morphogenetic movements leading to wing formation. Conversely, inconsistent with the normal disc development, a protracted in vivo culturing of an intact wing disc results in a predominant proportion of G1 cells (55%, data from Fain & Alvarez, 1987). Although there is no direct proof to demonstrate whether the cells participating in the regeneration process are initially in G2 or G1/G0, evidence exists in favour of the latter.…”

“…Although there is no direct proof to demonstrate whether the cells participating in the regeneration process are initially in G2 or G1/G0, evidence exists in favour of the latter. In Fain & Alvarez (1987), a significant increase in G2 cells was observed in dissociated and reaggregated imaginal disc cells cultivated in vivo for 12 hours. In addition, cultured imaginal disc fragments show a lag period of at least 12 hours before an increase in cell number is evident, suggesting that S-phase cells appear first (Adler 1981, Kiehle & Schubiger 1985 and further, comparison of blastema frequencies presented here (blastema present in 47% of the discs after 24 hours) and in O' Brochta & Bryant (1987) demonstrate the earlier appearance of blastemas visualized with S-phase cells.…”

“…This idea, largely based on the polar co-ordinate model developed by French et al (1976), is however impaired by the finding that, during normal development, discontinuity in cell fates does not result in additional growth (Chen & Struhl 1996, see Held 2002 for discussion) and further, that regeneration from an L1 anterior 1/4 fragment is dependent on the Hedgehog signal from the peripodial membrane rather than the interaction between the wound edges (Gibson & Schubiger 1999), the latter being in favour of the boundary model of Meinhardt (1983). DNA synthesis, induced by the disc fragmentation, has been clearly shown to precede homotypic wound healing (Dale & Bownes 1980, Bryant & Fraser 1988 and consequently it has been suggested that the cells next to the cut edge would arrest in G2 until their apposition by wound healing triggers the cells to enter mitosis (Fain & Alvarez 1987). However, at present it is not known how the cells near the cut edges are recruited into the cell cycle, nor is it even directly shown whether the cell divisions are regulated by the wound healing process.…”

“…the emerging of the new pattern is dependent on cell divisions taking place in a specialized proliferating tissue called the blastema. The dynamics of regenerative proliferation have been extensively studied by clonal analysis (Abbot et al 1981), incorporation of 3 H-thymidine into replicating cells (Dale & Bownes 1980, Adler 1984, Kiehle & Schubiger 1985, O'Brochta & Bryant 1987, direct cell counting (Dunne 1981), volume measurement of cultured disc fragments (Adler 1981), flow cytometric analysis (Fain & Alvarez 1987) and immunolocalization of incorporated bromodeoxyuridine (Bryant & Fraser 1988).…”

Cell death-induced regeneration in wing imaginal discs requires JNK signalling

“…As occurs in amphibian limbs, tadpole tails and zebrafish fins and heart (Brockes and Kumar, 2008;Galliot et al, 2008;Slack et al, 2008), a regeneration blastema forms after cutting a piece of the disc (Bryant, 1971;Bryant and Fraser, 1988;Schubiger, 1971) and, even when isolated, the blastema can regenerate the lost structure . These blastemas display localised proliferation near the wound edges and mitosis and DNA synthesis are observed in the tissue prior to completion of wound healing (Adler, 1981;Bosch et al, 2008;Bryant and Fraser, 1988;Dunne, 1981;Fain and Alvarez, 1987;O'Brochta and Bryant, 1987). However, relatively little is understood about the control of proliferation in these regenerating tissues.…”