Transcription Factors That Control Behavior—Lessons From C. elegans

Abstract

Behavior encompasses the physical and chemical response to external and internal stimuli. Neurons, each with their own specific molecular identities, act in concert to perceive and relay these stimuli to drive behavior. Generating behavioral responses requires neurons that have the correct morphological, synaptic, and molecular identities. Transcription factors drive the specific gene expression patterns that define these identities, controlling almost every phenomenon in a cell from development to homeostasis. Therefore, transcription factors play an important role in generating and regulating behavior. Here, we describe the transcription factors, the pathways they regulate, and the neurons that drive chemosensation, mechanosensation, thermosensation, osmolarity sensing, complex, and sex-specific behaviors in the animal model Caenorhabditis elegans. We also discuss the current limitations in our knowledge, particularly our minimal understanding of how transcription factors contribute to the adaptive behavioral responses that are necessary for organismal survival.

Dauer quiescence as well as continuity of the life cycle after dauer-exit in Caenorhabditis elegans are dependent on the endoribonuclease activity of XRN-2

“…MEC-3, a LIM-homeobox TF, plays a critical role in the terminal differentiation of mechanosensory neurons such as AVM, ALMs, PVM, PLMs, FLPs, and PVDs and is required for touch response behaviour 59–63, 67 . TFs, UNC-86 and LIN-32 are the major developmental regulators of MEC-3-expressing neurons.…”

“…Finally, HSN motor neurons can control egg-laying through G protein-coupled receptor-mediated regulation of vulval muscle contraction 72, 76 . UNC-86, HLH-3, EGL-18, AST-1, CEH-20, SEM-4 and EGL-46 collectively control terminal differentiation and function of HSN neurons 59, 61–63, 72, 76 . Together, these TFs induce and maintain HSN-expressed genes, including tph-1 and cat-1 , where UNC-86 acts as the master regulator for most of the other TFs.…”

“…4A ). Zinc finger TF, CHE-1, along with CEH-36 drives the fate and chemotaxis properties of the ASE neurons, whereas UNC-30 plays a key role in the functionality of ASG neurons 59–63, 65 . UNC-3, a member of the Collier/Olf1/EBF (COE) TF family, induces the effector genes required for the maintenance of ASI neuron fate and functionality 59, 61, 62 .…”

“…The AIY interneurons receive and integrate information from several amphid sensory neurons, including AWA, AWB, AFD, and ASE, and are involved in locomotion, thermotaxis and chemotaxis 63, 68 . A complex comprising TTX-3 [LIM homeobox 9 (LHX9) ortholog], and CEH-10 [human visual system homeobox 2 (VSX2) ortholog] along with CEH-23 control AIY neuron terminal differentiation 59–63 . These candidates are involved in an induction cascade as depicted in Fig.…”

“…The AIZ interneurons are involved in the odorant sensing pathway and receive signals from the AWA and AWC chemosensory neurons. UNC-86 induces AIZ generation during embryogenesis and is required to maintain AIZ function throughout life 59–63 . As mentioned earlier, unc-86 mRNA got downregulated in experimental dauers suggesting that AIZ neuronal maintenance might got compromised, which in turn might have resulted in defective odor-attraction and odor-adaptation behavior in them.…”