Department of Biology, Hopkins Marine Station of Stanford University, Pacific Grove, CA 93950
The polarity of the C. elegans P7.p cell divisions is controlled by the Wnt/β-catenin asymmetry pathway (Green et al., 2008; Minor et al., 2013). This pathway includes the β-catenin-like proteins SYS-1 and WRM-1, POP-1/TCF, and the Nemo-like-kinase, LIT-1 (reviewed by Mizumoto and Sawa, 2007). The Wnt/β-catenin asymmetry pathway ensures different ratios of SYS-1 to POP-1, controlling the differential transcription of Wnt target genes between daughters of an asymmetric cell division. Because our genetic data indicate an antagonism between LRP-2 and LIN-17 similar to that between CAM-1 and VANG-1 and LIN-17 (Minor and Sternberg, 2019), we wanted to determine if LRP-2 can control the asymmetric localization of SYS-1 between the daughter cells of P7.p during anaphase of the first cell division. The initial establishment of vulval polarity can be observed through the localization of VENUS::SYS-1 (VNS::SYS-1), localized in a high (P7.pa)/low (P7.pp) pattern in the wild-type worm, reciprocal to the localization of POP-1/TCF (Phillips et al., 2007; Green et al., 2008).
It was previously reported (Green et al. 2008) that VNS::SYS-1 asymmetry in P7.p daughter cells is often lost in lin-17(n671) and lin-18(e620) mutants. These mutants display two aberrant patterns of VNS::SYS-1 localization as well as the wild-type pattern, though less frequently. The two deviant localization patterns include one in which both P7.pa and P7.pp express equal amounts of VNS::SYS-1 and a reversed VNS::SYS-1 pattern in which P7.pp is enriched with VNS::SYS-1. By observing VNS::SYS-1 localization in a lin-17(n671); lrp-2(gk272) background we see that the aberrant localization of SYS-1 is suppressed to a similar degree to that of lin-17(n671); cam-1(gm122) and lin-17(n671); vang-1(ok1142). This observation confirms LRP-2 controls vulval cell polarity by antagonizing LIN-17 in a similar fashion to CAM-1 and VANG-1, and that the effect of LRP-2 is at the level of P7.p rather than its progeny.
MT1306: lin-17(n671) (Ferguson and Horvitz, 1985)
MT1488: lin-17(n671); unc-13(e1091)
PS5840: lin-17(n671); cam-1(gm122); qIs95[pSYS-1::VENUS::SYS-1] (Green et al., 2008)
PS5787: lin17(n671); vang-1(ok1142); qIs95[pSYS-1::VENUS::SYS-1] (Green et al., 2008)
The lin17(n671); lrp-2(gk272) double mutant was constructed by crossing VC543 lrp-2(gk272) males with strain MT1488: lin-17(n671); unc-13(e1091) hermaphrodites.
JK4062: lin-17(n671); qIs95[pSYS-1::VENUS::SYS-1]
The lin17(n671); lrp-2(gk272); qIs95[pSYS-1::VENUS::SYS-1] line was created by crossing VC543 lrp-2(gk272) males with JK4062: lin-17(n671); qIs95[pSYS-1::VENUS::SYS-1] hermaphrodites
Howard Hughes Medical Institute, with whom PWS was an Investigator. The National Institute of Neurological Disorders and Stroke of the National Institutes of Health under award number 1F32NS098658-01A1 awarded to PJM.
Reviewed ByHitoshi Sawa
HistoryReceived: July 29, 2019
Accepted: August 27, 2019
Published: August 27, 2019