Genetic markers enable the verification and manipulation of the dauer entry decision

Abstract

Phenotypic plasticity allows animals to survive in changing environments through the alteration of phenotypes or development. One of the best-studied examples of phenotypic plasticity is dauer larval development in the free-living roundworm Caenorhabditis elegans. When faced with hostile environments, C. elegans larvae can exit reproductive development and enter the stress-resistant and spore-like dauer larval stage. However, knowledge about how the dauer entry decision is made, and how the different tissues of the animal coordinate to execute transformation into dauer, is limited. This is because identifying animals that make the entry decision, or that fail to coordinately remodel their tissues during dauer development, is time-consuming and labor-intensive. Utilizing our previously reported RNA-seq of animals going through dauer or reproductive development (Lee et al., 2017), we have identified genetic markers for conveniently tracking and manipulating the dauer entry decision. These include col-183 (which tracks dauer fate in the hypodermis), ets-10 (neurons and intestine), nhr-246 (intestine and hypodermis), and F53F1.4 (reproductive fate in the hypodermis). Using condition shift experiments, we demonstrate that the dauer-specific fluorescent expression of the markers correspond to the commitment event of the dauer entry decision, and therefore label when the decision is made. We show that these markers can be used to manipulate the entry decision by driving the reproduction-promoting gene daf-9 under the control of the dauer-specific marker col-183, through which we could shift animals into nondauer development. We further demonstrate that the markers can be used to track tissue coordination during the decision. daf-9, daf-15, and daf-18 partial dauers exhibit incomplete expression of the ets-10 marker, with our results indicating that the same gene (e.g. daf-9 or daf-18) can affect dauer development differently in different tissues. Our findings provide molecular tools for studying phenotypic plasticity during a whole animal decision.

Mutually exclusive dendritic arbors in C. elegans neurons share a common architecture and convergent molecular cues

“…Indeed, we found that the daf-15 mutants fail to display dauer-specific expression of lag-2p::gfp in the IL2 cell bodies (Fig 5H). This corresponds with a recent publication demonstrating reduction of dauer-specific expression of ets-10p::gfp in a daf-15 background [55]. To our surprise, the daf-15 partial dauer FLPs had extensive arborization (Fig 5G).…”

Stress-induced dendritic branching inC. elegansrequires both common arborization effectors and stress-responsive molecular pathways

“…Given the lack of dauer-specific features, we question whether these were true dauers. A recent publication showing reduction of dauer-entry expression of the ets-10p::gfp transgene in a daf-15 background (51). Additional experiments will be required to understand the possible interactions of DAF-18 and DAF-15 in IL2 arborization.…”

SLC17A6/7/8 Vesicular Glutamate Transporter Homologs in Nematodes

“…In light of the downregulation and redistribution of VGLU-2::GFP in dauers, it is notable that animals that enter the dauer arrest stage substantially remodel their cuticle and collagen composition (Cox et al 1981;Cox and Hirsh 1985;Kramer et al 1985;Lee et al 2017;Shih et al 2019). VGLU-2 expression changes may be required for these remodeling events.…”