Fig. 8: A proposed working model of PRMT7 during lung alveolarization.

During lung alveolar morphogenesis, PRMT7 and H4R3me1 directly bind to the promoter of Foxm1 to activate its expression, and thereby promote the proliferation and differentiation of AMYFs. In the absence of PRMT7 and H4R3me1, repressed Foxm1 results in reduced proliferation and differentiation of AMYFs, compromised elastin deposition, failure of septa formation, and eventually form a lung with enlarged distal airspaces structures. The red star indicates the secondary septa.