“…C. elegans has nine α- and six β-tubulin genes in its genome ( C. elegans Sequencing Consortium, 1998; Gogonea et al. , 1999).…”
Section: Resultsmentioning
confidence: 99%
“…Of the other eight α- and five β-tubulins in the C. elegans genome ( C. elegans Sequencing Consortium, 1998; Gogonea et al. , 1999), previous investigators found evidence for the expression of two other α‑tubulins in the TRNs in addition to MEC‑12: tba‑1 and tba‑2 (Fukushige et al.…”
Microtubules contribute to key cellular processes and are composed of αβ-tubulin heterodimers. Neurons in Caenorhabditis elegans express cell type–specific isoforms in addition to a shared repertoire and rely on tubulins for neurite outgrowth. Isoform function varies between in vivo and in vitro contexts.
“…C. elegans has nine α- and six β-tubulin genes in its genome ( C. elegans Sequencing Consortium, 1998; Gogonea et al. , 1999).…”
Section: Resultsmentioning
confidence: 99%
“…Of the other eight α- and five β-tubulins in the C. elegans genome ( C. elegans Sequencing Consortium, 1998; Gogonea et al. , 1999), previous investigators found evidence for the expression of two other α‑tubulins in the TRNs in addition to MEC‑12: tba‑1 and tba‑2 (Fukushige et al.…”
Microtubules contribute to key cellular processes and are composed of αβ-tubulin heterodimers. Neurons in Caenorhabditis elegans express cell type–specific isoforms in addition to a shared repertoire and rely on tubulins for neurite outgrowth. Isoform function varies between in vivo and in vitro contexts.
“…In place of the dat-1 promoter, we tried to express cdc-25.4 transgenes under the control of the tba-9 promoter and the pkd-2 promoter to express cdc-25.4 in ray A-type and B-type neurons, respectively. tba-9 is one of the nine α tubulins and is expressed in various ciliated sensory neurons, including several male-specific neurons (Gogonea et al 1999; Hurd et al 2010). pkd-2 is expressed in male-specific sensory neurons and required for male mating behavior (Barr and Sternberg 1999; Barr et al 2001).…”
Cell division cycle 25 (cdc25) is an evolutionarily conserved phosphatase that promotes cell cycle progression. Among the four cdc25 orthologs in Caenorhabditis elegans, we found that cdc-25.4 mutant males failed to produce outcrossed progeny. This was not caused by defects in sperm development, but by defects in male mating behavior. The cdc-25.4 mutant males showed various defects during male mating, including contact response, backing, turning, and vulva location. Aberrant turning behavior was the most prominent defect in the cdc-25.4 mutant males. We also found that cdc-25.4 is expressed in many neuronal cells throughout development. The turning defect in cdc-25.4 mutant males was recovered by cdc-25.4 transgenic expression in neuronal cells, suggesting that cdc-25.4 functions in neurons for male mating. However, the neuronal morphology of cdc-25.4 mutant males appeared to be normal, as examined with several neuronal markers. Also, RNAi depletion of wee-1.3, a C. elegans ortholog of Wee1/Myt1 kinase, failed to suppress the mating defects of cdc-25.4 mutant males. These findings suggest that, for successful male mating, cdc-25.4 does not target cell cycles that are required for neuronal differentiation and development. Rather, cdc-25.4 likely regulates noncanonical substrates in neuronal cells.
“…The C. elegans genome encodes nine α and six β tubulins [80, 81]. The α-tubulin TBA-6 is expressed in the IL2 neurons and polycystin-expressing neurons, but absent from amphid and phasmid ciliated neurons [81].…”
Section: Elegans Cilia Are Specialized In Form and Functionmentioning
The investigation of C. elegans males and the male-specific sensory neurons required for mating behaviors has provided insight into the molecular function of polycystins and mechanisms that are needed for polycystin ciliary localization. In humans, polycystin 1 and polycystin 2 are needed for kidney function; loss of polycystin function leads to autosomal dominant polycystic kidney disease (ADPKD). Polycystins localize to cilia in C. elegans and mammals, a finding that has guided research into ADPKD. The discovery that the polycystins form ciliary receptors in male-specific neurons needed for mating behaviors has also helped to unlock insights into two additional exciting new areas: the secretion of extracellular vesicles; and mechanisms of ciliary specialization.
First, we will summarize the studies done in C. elegans regarding the expression, localization, and function of the polycystin 1 and 2 homologs, LOV-1 and PKD-2, and discuss insights gained from this basic research. Molecules that are co-expressed with the polycystins in the male-specific neurons may identify evolutionarily conserved molecular mechanisms for polycystin function and localization.
We will discuss the finding that polycystins are secreted in extracellular vesicles that evoke behavioral change in males, suggesting that such vesicles provide a novel form of communication to conspecifics in the environment. In humans, polycystin-containing extracellular vesicles are secreted in urine and can be taken up by cilia, and quickly internalized. Therefore, communication by polycystin-containing extracellular vesicles may also use mechanisms that are evolutionarily conserved from nematode to human.
Lastly, different cilia display structural and functional differences that specialize them for particular tasks, despite the fact that virtually all cilia are built by a conserved Intraflagellar Transport (IFT) mechanism and share some basic structural features. Comparative analysis of the male-specific cilia with the well-studied cilia of the amphid and phasmid neurons has allowed identification of molecules that specialize the male cilia. We will discuss the molecules that shape the male-specific cilia. The cell biology of cilia in male-specific neurons demonstrates that C. elegans can provide an excellent model of ciliary specialization.
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