Caenorhabditis elegans Neural Development


The nervous system of the nematode Caenorhabditis elegans has been well described in terms of cell lineage, neural anatomy and connectivity. Identifying mutations that disrupt these defining characteristics has led to a detailed understanding of the genetic and molecular mechanisms of neural development in C. elegans.

Keywords: caenorhabditis elegans; nervous system; genetics; cell lineage; homeodomain; LIM‐domain

Figure 1.

The nervous system of the C. elegans hermaphrodite. (a) Schematic representation of the neuronal cell bodies in the head (green circles), ventral cord (red circles), tail (blue circles) and lateral positions (black circles) in the adult hermaphrodite. The worm is shown lying on its right side and therefore only neurons on the left side or middle of the worm are represented. (b) Confocal image of a transgenic worm that expressed GFP in the nervous system under the regulation of a pan‐neuronal promoter. Neuronal cell bodies in the head and tail, and in ventral and lateral positions are evident, as are the neural processes of the ventral, lateral and dorsal nerve cords. Commissures running circumferentially can also be seen.

Figure 2.

Cell differentiation in the lineages of the P neuroblasts. (a) Schematic of a hermaphrodite showing the approximate position of the P neuroblasts along the ventral cord (filled ovals). Below are the patterns of cell division and differentiation of P1–P12. The vertical lines connect to horizontal lines that represent division of the cell shown above. X indicates programmed cell death. (b) Expression pattern of lin‐39 (red underline), mab‐5 (blue underline) and egl‐5 (yellow underline) in the P cell lineages. Those cells that express both lin‐39 and mab‐5 are shown in purple and those that express both mab‐5 and egl‐5 are shown in green. To demonstrate that patterning along the A/P axis is lost in lin‐39, mab‐5 and egl‐5 mutants, the identity of neurons affected by these mutations is shown. Mutations in lin‐39 affect P3–P8, mutations in mab‐5 affect P11 and P12, and mutations in egl‐5 affect P12.

Figure 3.

Differentiation of the touch cells. (a) Schematic diagram of a worm showing the approximate locations of the neuronal cell bodies (circles) of the touch cells and their processes (lines). Neurons in red mediate backwards avoidance responses, while those in green mediate forward avoidance responses. (b) Genetic pathway for touch cell differentiation. vab‐15 is thought to act upstream of lin‐32, which activates expression of unc‐86. unc‐86 drives mec‐3 expression, which in turn regulates mec‐4 and mec‐7. mec‐3 also maintains its own expression by autoregulation. lin‐22 restricts touch cell differentiation in other neurons by negatively regulating lin‐32. (c) Cell division in the Q neuroblasts. Red lines indicate cells that express UNC‐86 in wild‐type worms. Grey lines represent cells that no longer express unc‐86 in mutant worms.

Figure 4.

Amphid sensory neurons and the differentiation of AWA, AWB and AWC. (a) Schematic of an adult hermaphrodite and the approximate position of neuronal cell bodies of the amphid neurons (filled circles) and their processes (lines). (b) Labelled cell bodies of the amphid neurons. Anterior is to the left and posterior to the right. Only neurons on the left side of the worm are represented. Neurons in red are involved in the repulsion from specific chemical compounds, while those in green are required for attraction. The ASJ neurons, as well as ASI, ADF and ASG, are involved in detecting sensory cues that regulate the entry and exit from an alternative larval stage called the dauer state. (c) Differentiation of AWA (yellow), AWB (purple) and AWC (blue). Black text represents genetic pathways that lead to the appropriate differentiation of the AWA, AWB and AWC neurons. Pathways in red text indicate those in either lin‐11, lim‐4 or odr‐7 mutants that lead to inappropriate differentiation of the AWC default state.


Further Reading

Antebi A, Norris CR and Hedgecock EM (1997) Cell and growth cone migrations. In: Riddle DL, Blumenthal T, Meyer BJ and Priess JR (eds) C. elegans II, pp. 583–609. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press.

Bargmann CI, Hartwieg E and Horvitz HR (1993) Odorant‐selective genes and neurons mediate olfaction in C. elegans. Cell 74: 515–527.

Chalfie M (1995) The differentiation and function of the touch receptor neurons of Caenorhabditis elegans. Progress in Brain Research 105: 179–182.

Hobert O and Westphal H (2000) Functions of LIM‐homeobox genes. Trends in Genetics 16: 75–83.

Livesey FJ (1999) Netrins and netrin receptors. Cell and Molecular Life Sciences 56: 62–68.

Ruvkan G (1997) Patterning the nervous system. In: Riddle DL, Blumenthal T, Meyer BJ and Priess JR (eds) C. elegans II, pp. 543–581. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press.

Sulston JE and Horvitz HR (1977) Post‐embryonic cell lineages of the nematode, Caenorhabditis elegans. Developmental Biology 56: 110–156.

Sulston JE, Schierenberg E, White JG and Thomson JN (1983) The embryonic cell lineage of the nematode Caenorhabditis elegans. Developmental Biology 100: 64–119.

Tessier‐Lavigne M and Goodman CS (1996) The molecular biology of axon guidance. Science 274: 1123–1133.

White JG, Southgate E, Thomson JN and Brenner S (1986) The structure of the nervous system of the nematode Caenorhabditis elegans. Philosophical Transactions of the Royal Society of London 314B: 1–340.

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Brockie, Penelope J, and Maricq, Andres V(Mar 2003) Caenorhabditis elegans Neural Development. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0000792]