Role of Toll Receptors in Tribolium
Knockdown of two Toll family receptors in Tribolium disrupts cell rearrangements in the early embryo (Benton et al., 2016), although cell movements in later embryos were not examined. These experiments led to the hypothesis that, like Drosophila, the pair-rule genes are regulatory intermediates in a cascade that regulates cell rearrangements at least in part through the activity of Toll family receptors (Benton et al., 2016). There are, however, significant differences in how and when the Toll stripes are expressed relative to cell movements in both species. In Drosophila, each segmental anlage is four cells wide and each cell row has a distinct combination of Toll receptor expression, with proposed heterophilic interactions between cell rows. The differential expression is established prior to any of the movements of germband elongation (Pare et al., 2014). In Tribolium, a stripe of double segment periodicity (between five and six cells wide) of Toll7 is flanked by a stripe of double segment periodicity of TolllO, thus very few rows of cells would experience heterophilic interactions. In addition, these stripes are added sequentially from the posterior, while the embryo is elongating. Whether cells express different Toll receptors prior to the onset of their cell movements or whether Toll receptor interactions drive differential accumulation of actomyosin is not known. In sum, whether the same cellular mechanisms underlie the loss of function phenotypes in both species remains unclear.
Polarized Effectors of Cell Movement Have Not Been Documented in Tribolium
In Drosophila, subcellular polarized distribution of motor or adhesion proteins is required for normal apical junctional remodeling (reviewed in Zallen, 2007; Zallen and Blankenship, 2008): myosin II, F-actin, DE-cadherin, armadillo/|3-catenin, and Bazooka/PAR-3. Similarly, actin and lipid phosphatidyl inositol 3,4,5-trisphosphate (which promotes actin polymerization) are found in basolateral protrusions (Sun et al., 2017). In Tribolium, polarized candidates have yet to be reported. Furthermore, RNAi and CRISPR knockdowns of the Tribolium homolog of E-cadherin are reported to have no effect on either elongation or segmentation, although they disrupt dorsal closure (Gilles et al., 2015). Interestingly, the mutant larva illustrated publication are significantly shorter than the wild-type.
In Drosophila germband extension, PCP pathway genes are not required (Zallen and Wieschaus, 2004). Flowever, in Tribolium, preliminary knockdowns of PCP (flamingo, fat, and dachsous) and JNK (basket and hemipterous) pathway regulators produce larval cuticle phenotypes that include truncation and failure of dorsal closure (Fu, 2014). Since many cuticles were empty, Fu (2014) also analyzed embryonic phenotypes and found evidence that PCP pathway genes were required for proper embryo condensation from the blastoderm. While preliminary, these data suggest a possible role for PCP genes in convergent extension in Tribolium at both early and late stages, in contrast to the lack of PCP regulation in Drosophila germband extension.