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. Author manuscript; available in PMC: 2017 Jul 23.
Published in final edited form as: Dev Biol. 2016 Jul 28;419(1):121–131. doi: 10.1016/j.ydbio.2016.07.020

Fig 5.

Fig 5

Asymmetrically activated MAPK signaling in muscle satellite cell ACD and Arabidopsis stomatal ACD. (A) Asymmetric p38α/β MAPK activity in mouse muscle satellite cell ACD. Polarized PAR protein complex activates p38α/β MAPK activity in only one daughter cell, which turns on the expression of bHLH transcription factor MyoD to promote amplifying divisions followed by terminal fate differentiation. The other daughter cell exits cell division and returns to the quiescent state. (B)Asymmetric distribution of the YDA-MPK3/6 cascade in Arabidopsis stomatal ACD. Premitotically polarized BASL-YDA-MPK3/6 complex is only inherited to the large daughter cell (SLGC, stomatal lineage ground cell), which results in phosphorylation of the nuclear bHLH SPCH for degradation. Differential SPCH expression levels in two daughters direct their distinct developmental path. The small daughter (M, Meristemoid) undergoes a few divisions and terminates into stomatal guard cells and the large SLGC expands to become a pavement cell (PC).