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Comment
. 2016 Mar 30;5(2):e1170274.
doi: 10.1080/21624054.2016.1170274. eCollection 2016 Apr-Jun.

The adhesion GPCR latrophilin - a novel signaling cascade in oriented cell division and anterior-posterior polarity

Jana Winkler  1 , Simone Prömel  1
Affiliations
Comment

The adhesion GPCR latrophilin - a novel signaling cascade in oriented cell division and anterior-posterior polarity

Jana Winkler et al. Worm. .

Abstract

Although several signaling pathways in oriented cell division have been well characterized such as delta/notch inductions or wnt/frizzled-based anterior-posterior polarity, there is strong evidence for additional signal pathways controlling early anterior-posterior polarity decisions. The homolog of the adhesion G protein-coupled receptor latrophilin, LAT-1 has been identified as a receptor essential for oriented cell division in an anterior-posterior direction of specific blastomeres in the early C. elegans embryo. We recently conducted a study aiming at clarifying the signals involved in LAT-1 function. We identified a Gs protein/adenylyl cyclase/cAMP pathway in vitro and demonstrated its physiological relevance in oriented cell division. By interaction with a Gs protein LAT-1 elevates cAMP levels. These data indicate that G-protein signaling in oriented cell division is not solely GPCR-independent. This commentary will discuss our findings in the context of the current knowledge of mechanisms controlling oriented cell division and anterior-posterior polarity. Further, we identify open questions which need to be addressed in the future.

Keywords: G protein-coupled receptor; early C. elegans embryo; latrophilin; signaling pathway; spindle orientation.

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Figures

Figure 1.
Figure 1.
Schematic depiction of cleavage plane orientations in early wild-type and lat-1 mutant C. elegans embryos. In the 8-cell stage of wild-type embryos, ABal divides in a 128° angle to the anterior-posterior axis. This slightly skewed angled leads to the arising daughter cell ABala being displaced to the most anterior location of the embryo not contacting the MS blastomere whereas the ABalp daughter touches its posterior neighbor MS. In lat-1 mutant individuals the ABal cleavage plane is displaced to approximately 90° resulting in ABalp and ABala blastomeres which both contact MS.
Figure 2.
Figure 2.
Model of LAT-1 signaling. In the absence of an extracellular agonist LAT-1 resides in an inactive state. As a consequence of interaction of LAT-1 with a so far unknown agonist, LAT-1 is activated by an intramolecular sequence in the extracellular domain adjacent to the transmembrane domain. This sequence possibly interacts with the 7 transmembrane domain. Due to further conformational changes a Gαs protein dissociates from its βγ subunit and is able to activate adenylyl cyclases (AC) which subsequently produce cAMP. This second messenger is essential for the control of correct cell division plane orientation in the ABal bastomere.
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