Fig. 2
knon mutants exhibit aberrant Nebenkern structure and defective mitochondrial elongation that can be suppressed by bypassing mitochondrial fusion. a Phase-contrast micrograph of early elongation-stage spermatids from knon ms(2)1400 ; fzo 1 males show some degree of elongation of unfused mitochondria (arrows); compare to Fig. 1c-d. b-e Cross sections of elongating spermatids viewed by transmission electron microscopy showing axonemes (arrowheads) and elongating mitochondrial derivatives (arrows). Wild-type spermatids (b) show two mitochondrial derivatives per axoneme. c knon ms(2)1400 spermatids lack detectable mitochondrial derivatives beside the axoneme. d fzo 1 spermatid has multiple mitochondrial derivatives per axoneme resulting from failure of mitochondrial fusion to form the Nebenkern [3]. e Spermatid from knon ms(2)1400 ; fzo 1 male shows several mitochondrial derivatives elongating beside the axoneme. Transmission electron micrographs of cross sections of Nebenkerne from wild-type (f) and knon ms(2)1400 (g) males. Two examples of each are shown. Internal “onion” structure is disrupted in knon ms(2)1400 . Scale bars 20 μm in a, 0.5 μm in b-e, and 2 μm in f-g. b and d adapted from [3]