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Fig. 5. PtdIns(4,5)P₂ depletion affects axoneme architecture. (A-C) Transmission electron micrographs (TEMs) showing the distribution of axonemes (arrowheads) in spermatid cysts. (A) Wild-type cysts have many axonemes with a regular 9 + 2 arrangement (inset, magnified axoneme). (B) Spermatid cysts expressing SigD have few axonemes, and these axonemes have aberrant MT organization (inset). (C) Co-expression of Sktl with SigD restores axonemes of normal architecture (inset). (D-I) TEMs showing axonemal architecture and axial membranes. Major (m1) and minor (m2) mitochondrial derivatives are indicated. (D,G) Wild-type axonemes. (D) Wild-type spermatids have doublet MTs (arrow) surrounded by axial membranes (triple arrows) adjacent to the two mitochondrial derivatives. (G) Axonemes from later-stage spermatids develop accessory MTs that are centripetally displaced from the outer doublet MTs (inset, arrow). (E,H) Axonemes from SigD-expressing spermatids. (E) Note the presence of triplet MTs (arrow). (H) Axial membranes (triple arrows) fail to ensheath axonemes that are falling apart (arrowhead). No SigD axonemes with accessory MTs were observed. (F,I) Co-expression of Sktl with SigD restored axonemal doublets and accessory MTs (arrow, I); however, occasional defects in doublet orientation were observed (arrow, F). Scale bars: 500 nm (A-C), 100 nm (D-I).

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