The axoneme is the basic functional unit of the eucaryotic flagellum. Periodic structures appended to its 9+2 microtubule core are responsible for generation of flagellar bending. An account of biochemical and genetic studies of flagellar-defective mutants of Chlamydomonas reinhardtii is presented. These studies provide insights into the complex molecular composition of the appended structures, their mode of assembly, and the way in which they interact to modulate flagellar function.

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Genetic and biochemical dissection of the eucaryotic flagellum.

https://www.cell.com/cell/pdf/0092-8674(82)90436-6.pdf

Uniflagellar mutants of Chlamydomonas: evidence for the role of basal bodies in transmission of positional information.

1 Introduction.- 1.1 Why is movement interesting?.- 1.2 What do we mean by 'movement'?.- 1.3 What causes movement?.- 1.4 An analogy.- 1.5 Motor design - an abstract exercise.- 1.6 How are movements controlled?.- 1.7 Which motor for the task?.- References.- 2 Motors Based on Actomyosin.- 2.1 Introduction.- 2.2 Components of the motor.- 2.3 The basic motor.- 2.4 Linear contractile systems.- 2.5 Non-linear: planar systems.- 2.6 Non-linear: solid systems.- 2.7 Control of the motor.- 2.8 Summary.- References.- 3 Motors Based on Microtubules.- 3.1 Introduction.- 3.2 Structure of microtubules.- 3.3 Dynein.- 3.4 The basic motor.- 3.5 Cilia and flagella.- 3.6 Movement in the mitotic spindle.- 3.7 Movement associated with cytoplasmic microtubules.- 3.8 Summary.- References.- 4 Motors of Other Sorts.- 4.1 Introduction.- 4.2 Bacterial flagella.- 4.3 Other bacterial motors.- 4.4 The spasmoneme of vorticellids.- 4.5 Assembly-disassembly motors.- 4.6 Hydraulic systems.- 4.7 Miscellaneous motor systems.- 4.8 Summary.- References.- 5 Swimming.- 5.1 General.- 5.2 Swimming.- 5.3 Methods of obtaining forward thrust.- 5.4 Control of the direction of ciliary beat.- 5.5 Summary.- References.- 6 Crawling Movement.- 6.1 Introduction.- 6.2 A simplistic analysis of the problem.- 6.3 Amoeba.- 6.4 Fibroblast locomotion.- 6.5 Fibroblast spreading.- 6.6 Movement of other cell types.- 6.7 Summary.- References.- 7 Moving in a Uniform Environment.- 7.1 Introduction.- 7.2 Random walks and internal bias.- 7.3 Effects of changes in environmental properties.- 7.4 Roughness.- 7.5 Rigidity and deformability.- 7.6 Summary.- References.- 8 Anisotropic Environments.- 8.1 General.- 8.2 Trapping and avoidance.- 8.3 Gradients.- 8.4 Flow.- 8.5 Magnetic and electric fields.- 8.6 Gravity.- 8.7 Shape.- 8.8 Rigidity.- 8.9 Summary.- References.- 9 Chemotaxis.- 9.1 General.- 9.2 The problem - a theoretical analysis.- 9.3 Bacterial Chemotaxis.- 9.4 Chemotaxis in Paramoecium.- 9.5 Chemotaxis in the cellular slime-moulds.- 9.6 Chemotaxis in Myxobacteria.- 9.7 Chemotaxis of leucocytes.- 9.8 Summary.- References.- 10 Cell-Cell Interactions.- 10.1 Introduction.- 10.2 Contact inhibition of locomotion.- 10.3 Consequences of contact inhibition.- 10.4 Escape from normal contact inhibition.- 10.5 Invasiveness as a general phenomenon.- 10.6 Summary.- References.

Cell Movement and Cell Behaviour

Primary ciliary dyskinesia (PCD) is a multisystem disease characterized by recurrent respiratory tract infections, sinusitis, bronchiectasis and male subfertility, associated in about 50% patients with situs inversus totalis (the Kartagener syndrome). The disease phenotype is caused by ultrastructural defects of respiratory cilia and sperm tails. PCD is a heterogenetic disorder, usually inherited as an autosomal recessive trait. So far, mutations in two human genes have been proved to cause the disease. However, the pathogenetics of most PCD cases remains unsolved. In this review, the disease pathomechanism is discussed along with the genes that are or may be involved in the pathogenesis of primary ciliary dyskinesia and the Kartagener syndrome.

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Primary ciliary dyskinesia: genes, candidate genes and chromosomal regions.

Mutations at three independent loci in Chlamydomonas reinhardtii result in a striking alteration of cell motility. Mutant cells representing the three mbo loci move backwards only, propelled by a symmetrical "flagellar" type of bending pattern. The characteristic asymmetric "ciliary" type of flagellar bend pattern responsible for forward movement that predominates in wild-type cells is seldom seen in the mutants. This defect in motility was found to be a property of the mutant axonemes themselves: the isolated axonemes, reactivated by addition of ATP, showed exclusively the symmetrical wave form, and the protein composition of these axonemes differed from the wild-type composition. Axonemes obtained from mbo1 , mbo2 , and mbo3 cells were found to be deficient in six polypeptides regularly present in wild type. The mbo2 axonemes were deficient in two additional polypeptides. The polypeptides were identified in autoradiograms of two-dimensional SDS polyacrylamide gel electrophoretograms of 35S- or 32P-labeled axonemes. One of the six polypeptides has previously been identified; it is a component missing in a mutant deficient for inner dynein arms. Of the five axonemal polypeptides newly identified by the mbo mutants, four were shown to be present as phosphoproteins in wild-type axonemes. One of the additional polypeptides deficient in mbo2 axonemes was also shown to be phosphorylated in wild-type axonemes. Detailed ultrastructural analysis of the mbo1 flagella and the mbo1 , mbo2A , and mbo3 axonemes revealed that the mutants specifically lack the beak-like projections found within the B-tubules of outer doublets 5 and 6.

/pdf/mutant-strains-of-chlamydomonas-reinhardtii-that-move-59txp80p0q.pdf

Huang B

Papers

Genetic and biochemical analysis of the eukaryotic flagellum.