Heterogeneity along the length has been well-documented in Chlamydomonas, with some inner dynein arms only present in a short proximal region and others in the remaining middle and distal regions (Yagi and Kamiya), and outer arms differing between the proximal and distal half of mammalian cilia (Omran and colleagues).  Circumferential heterogeneity, if it exists, may be post-translational, but alternatively inhomogeneity may reflect regulation of identical dyneins by doublet-specific mechanisms.  Adding extracted dyneins onto mutant axonemes that lack a single dynein might randomize circumferential modifications.  A similar homogenizing effect was seen for differences in motility of cis vs trans flagella in Chlamydomonas, traced to outer arm docking site differences (Takada and Kamiya, 1997).

Thank you so much David for your detailed answer. I am very well aware of the Yagi and Kamiya paper, that demonstrates dynein heterogeneity in Chlamydomonas flagella. However, I dont think the methodology followed in that paper can be applied to my research problem.

I have data that indicates dynein heterogeneity in a trypanosome flagellum. Using dynein inhibitors I have observed that the ciliary waveform of the flagellum is more strongly inhibited compared to the flagellar waveform (which is less sensitive). All these observations are using reactivated axonemes. What would you suggest be the next experiment(s) to address the same giving more conclusive results? Basically I need to conclusively demonstrate that there are possibly two different conformations of the dyneins that are responsible for the flagellar and ciliary waveforms.

Aakash, how do your categories of 'ciliary' vs 'flagellar' waveform relate to the direction of wave propagation in Trypanosomes?  Knockdown of outer arms in Tryps blocks normal tip-to-base wave propagation, but not reverse-swimming base-to-tip propagation (e.g., Branche et al. 2006; Baron et al. 2007).  Does the inhibitor affect one direction more than another?  If applied to a strain that has been knocked down for ODAs, does the inhibitor no longer alter waveform?  (Not related to your question, but possibly also of interest, if the inhibitor mainly affects ODAs, does it induce 'randomization' of CP orientation the way that lack of ODAs does?)

Well the trypanosome I am working on is not as genetically malleable as  Trypanosoma (in the papers you have referred). In flagellated trypanosomes in general, the flagellar waveform is tip-to-base and symmetric in nature; while the ciliary waveform is base-to-tip and asymmetric (Gadelha et al, Cell Motility Cytoskeleton 2007).

Yes, the inhibitor affects one direction i.e. the ciliary waveform more than the flagellar waveform. ODA knockouts of this particular trypanosome are unavailable. So basically I'm stuck on how should i conclusively demonstrate the possible mechanism that is responsible for the two waveforms.

Somewhat similar, yet highly preliminary data has been reported (Alexander and Burns. 1983. Nature). They observed using a drug EHNA, the ciliary and flagellar waveforms are differentially inhibited.