Coordinated spatial and temporal expression of Hox genes during embryogenesis in the acoel Convolutriloba longifissura

Background: Hox genes are critical for patterning the bilaterian anterior-posterior axis. The evolution of their clustered genomic arrangement and ancestral function has been debated since their discovery. As acoels appear to represent the sister group to the remaining Bilateria (Nephrozoa), investigating Hox gene expression will provide an insight into the ancestral features of the Hox genes in metazoan evolution. Results: We describe the expression of anterior, central and posterior class Hox genes and the ParaHox ortholog Cdx in the acoel Convolutriloba longifissura. Expression of all three Hox genes begins contemporaneously after gastrulation and then resolves into staggered domains along the anterior-posterior axis, suggesting that the spatial coordination of Hox gene expression was present in the bilaterian ancestor. After early surface ectodermal expression, the anterior and central class genes are expressed in small domains of putative neural precursor cells co-expressing ClSoxB1, suggesting an evolutionary early function of Hox genes in patterning parts of the nervous system. In contrast, the expression of the posterior Hox gene is found in all three germ layers in a much broader posterior region of the embryo. Conclusion: Our results suggest that the ancestral set of Hox genes was involved in the anteriorposterior patterning of the nervous system of the last common bilaterian ancestor and were later co-opted for patterning in diverse tissues in the bilaterian radiation. The lack of temporal colinearity of Hox expression in acoels may be due to a loss of genomic clustering in this clade or, alternatively, temporal colinearity may have arisen in conjunction with the expansion of the Hox cluster in the Nephrozoa

Distinct roles of Rac GTPases and the UNC-73/Trio and PIX-1 Rac GTP exchange factors in neuroblast protrusion and migration in C. elegans

The Rac and Cdc42 GTPases as well as the multiple GTP exchange factors that regulate their activity have been implicated in the pathways that drive actin cytoskeleton reorganization, but the individual contributions of these molecules to cell migration remain unknown. Studies shown here examine the roles of CED-10/Rac, MIG-2/RhoG and CDC-42 in the migration of the QL and QR neuroblasts in C. elegans. CED-10/Rac was found to normally limit protrusion and migration, whereas MIG-2/RhoG was required for protrusion and migration. CED-10/Rac and MIG-2/RhoG also had redundant roles in Q protrusion and migration. Surprisingly, CDC-42 was found to have only weak effects on the protrusion and the migration. We found that a mutation of unc-73/Trio, which encodes a GEF for CED-10/Rac and MIG-2/RhoG, caused protrusions that were thin and filopodia-like, suggesting that UNC-73/Trio is required for robust lamellipodia-like protrusion. A screen of the 19 C. elegans Dbl homology Rho GEF genes revealed that PIX-1 was required for proper Q neuroblast protrusion and migration. Genetic analysis indicated that PIX-1 might act in the CED-10/Rac pathway in parallel to MIG-2/RhoG and that PIX-1 has redundant function with UNC-73/Trio in Q neuroblast protrusion and migration. These results indicate that Rho GTPases and GEFs have both unique and overlapping roles in neuronal migration

The roles of EGF and Wnt signaling during patterning of the C. elegans Bγ/δ Equivalence Group

<p>Abstract</p> <p>Background</p> <p>During development, different signaling pathways interact to specify cell fate by regulating transcription factors necessary for fate specification and morphogenesis. In <it>Caenorhabditis elegans</it>, the EGF-Ras and Wnt signaling pathways have been shown to interact to specify cell fate in three equivalence groups: the vulval precursor cells (VPCs), the hook competence group (HCG) and P11/12. In the VPCs, HCG and P11/12 pair, EGF and Wnt signaling positively regulate different Hox genes, each of which also functions during fate specification. In the male, EGF-Ras signaling is required to specify the Bγ fate within the Bγ/δ equivalence pair, while Notch signaling is required for Bδ fate specification. In addition, TGF-β signaling by <it>dbl-1/dpp</it> controls <it>ceh-13/labial/Hox1</it> expression in Bγ.</p> <p>Results</p> <p>We show that EGF-Ras signaling is required for Bγ expression of <it>ceh-13/labial/Hox1</it>. The transcription factors <it>lin-1/ETS</it> and <it>lin-31/Forkhead</it>, functioning downstream of the EGF pathway, as well as <it>sur-2/MED23</it> (a component of the Mediator complex) also control <it>ceh-13</it> expression in Bγ. In addition, our results indicate that <it>lin-44/Wnt</it>, <it>mom-2/Wnt</it> and <it>lin-17/Fz</it> are necessary to maintain the division of Bγ along a longitudinal axis. We also show that <it>dbl-1/dpp</it> acts either in parallel or downstream of EGF pathway to regulate <it>ceh-13/Hox1</it> expression in Bγ. Lastly, we find that a <it>dbl-1/dpp</it> null mutation did not cause any vulval or P12 defects and did not enhance vulval and P12 defects of reduction-of-function mutations of components of the EGF pathway.</p> <p>Conclusions</p> <p><it>ceh-13/labial/Hox1</it> expression in Bγ is regulated by the EGF pathway and downstream factors <it>lin-1/ETS lin-31/Forkhead</it> and <it>sur-2/MED23</it>. Wnt signaling is required for proper Bγ division, perhaps to orient the Bγ mitotic spindle. Our results suggest that <it>dbl-1/dpp</it> is not required for VPC and P12 specification, highlighting another difference among these EGF-dependent equivalence groups.</p