Increased phosphorylation of dynein IC IC138 correlates with decreases in flagellar microtubule sliding and phototaxis defects. To test the hypothesis that regulation of IC138 phosphorylation controls flagellar bending, we cloned the IC138 gene. IC138 encodes a novel protein with a calculated mass of 111 kDa and is predicted to form seven WD-repeats at the C terminus. IC138 maps near the BOP5 locus, and bop5-1 contains a point mutation resulting in a truncated IC138 lacking the C terminus, including the seventh WD-repeat. bop5-1 cells display wild-type flagellar beat frequency but swim slower than wild-type cells, suggesting that bop5-1 is altered in its ability to control flagellar waveform. Swimming speed is rescued in bop5-1 transformants containing the wild-type IC138, confirming that BOP5 encodes IC138. With the exception of the roadblock-related light chain, LC7b, all the other known components of the I1 complex, including the truncated IC138, are assembled in bop5-1 axonemes. Thus, the bop5-1 motility phenotype reveals a role for IC138 and LC7b in the control of flagellar bending. IC138 is hyperphosphorylated in paralyzed flagellar mutants lacking radial spoke and central pair components, further indicating a role for the radial spokes and central pair apparatus in control of IC138 phosphorylation and regulation of flagellar waveform. INTRODUCTIONOur goal is to determine the mechanisms that regulate ciliary and eukaryotic flagellar bending. Based on informative mutations in Chlamydomonas, and effective in vitro functional studies, a surprisingly complex array of different dynein motors is required for generation and control of normal ciliary and flagellar bending (Mitchell, 1994;Gibbons, 1995;Porter, 1996;Porter and Sale, 2000;DiBella and King, 2001;Kamiya, 2002). For example, the outer arm dyneins are homogeneous structures responsible for control of beat frequency and power required for movement (Satir et al., 1993;Brokaw, 1994;DiBella and King, 2001;Kamiya, 2002). The inner arm dyneins, however, are more complex, composed of at least seven different dynein subspecies precisely organized in a 96-nm repeat pattern along each doublet microtubule of the axoneme (Porter, 1996;Porter and Sale, 2000). Diverse data indicate the inner arm dyneins control the size and shape of the flagellar bend (Brokaw and Kamiya, 1987;Brokaw, 1994;Kamiya, 2002). The mechanism for control of flagellar waveform involves additional structures (e.g., radial spokes, central pair apparatus, and the dynein regulatory complex) and control of dynein phosphorylation (Porter and Sale, 2000;DiBella and King, 2001;Kamiya, 2002;Smith and Yang, 2004).The present study is focused on a single inner arm dynein, the I1 complex, also called the f-dynein (Goodenough et al., 1987;Piperno et al., 1990;Kagami and Kamiya, 1992;Porter et al., 1992). The I1 complex is a tripartite structure, or triad, located near the base of the S1 radial spoke, at the proximal end of the axonemal 96-nm repeat (Goodenough and Heuser, 1985;Piperno et al., 1990;Mastronar...

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