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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: FEBS Lett. 2017 Oct 10;591(21):3447–3458. doi: 10.1002/1873-3468.12860

Figure 4. Cardiac-specific knock-down of TRiC chaperonin subunits causes disorganization of actin- and myosin-containing myofibrils.

Figure 4

Immunofluorescence images of 1-week (A–F) and 3-week (G–L) old hearts probed with phalloidin (F-actin, red) and DAPI (blue, DNA). Cardiac specific knock-down of TRiC chaperonin (Cct4 or Cct7) resulted in severe disorganization of actin-containing myofibrils (C, E, asterisks) in 1-week old fly hearts. Severe myofibril disorganization was also observed upon cardiac-specific knock-down of TRiC chaperonin (Cct4 or Cct7) when probed with muscle myosin antibody (green, D, F, asterisks). More severe myofibril defects (actin-containing myofibril disorganization is represented with asterisks) were observed in 3-week old fly hearts (I, K). Cardiac specific knock-down of TRiC chaperonin (Cct4 or Cct7) when probed with muscle myosin antibody resulted in near complete loss of contractile circumferential myofibrils (CF) in 3-week old hearts, whereas non-contractile longitudinal myofibrils (LF) were still present (J, L). Scale bars are 20 μm.