Three new and remarkable species of mosses from China and the Philippines

Distichophyllum meizhii Tan & Lin and D. wanianum Tan & Lin (Hookeriaceae) collected from southwestern region of China are described as new to science. Also, Horikawaea redfearnii Tan & Lin is described as a new species based on collections from Hainan Island of China and Palawan Island of the Philippines. The sporophytic specimen of Horikawaea Nog. was collected for the first time and support a family placement in Pterobryaceae

Evolutionary Conservation of the Heterochronic Pathway in C. elegans and C. briggsae

Heterochronic genes control the sequence and timing of developmental events during four larval stages of Caenorhabitis nematodes. Mutations in these genes may cause skipping or reiteration of developmental events. C. briggsae is a close relative of C. elegans. These species have similar morphology and share the same ecological niche. C. briggsae undergoes the same developmental pathway consisting of four larval stages before reaching adulthood. It also has the same set of heterochronic genes. Lin-28 is one of the heterochronic genes that also exists in other animals from flies to humans. It conservatively blocks the maturation of let-7 miRNA, the process is generally associated with the stem cell state. lin-28 is silenced as cells differentiate. C. elegans mutants of lin-28 have a reduced number of seam cells and precocious alae. Despite the highly conserved protein sequence, C. briggsae develop a distinct phenotype when its lin 28 is disrupted. Worms did not have a characteristic vulval development defect, they also became lethargic and had a reduced fertility. This observation led to a question of how conserved the heterochronic pathway is in close species

Monotonicity and 1-dimensional symmetry for solutions of an elliptic system arising in Bose-Einstein condensation

We study monotonicity and 1-dimensional symmetry for positive solutions with algebraic growth of the following elliptic system: $$\begin{cases} -\Delta u = -u v^2 & \text{in $\R^N$}\\ -\Delta v= -u^2 v & \text{in $\R^N$}, \end{cases}$$ for every dimension $N \ge 2$. In particular, we prove a Gibbons-type conjecture proposed by H. Berestycki, T. C. Lin, J. Wei and C. Zhao

Centro-affine normal flows on curves: Harnack estimates and Ancient solutions

We prove that the only compact, origin-symmetric, strictly convex ancient solutions of the planar $p$ centro-affine normal flows are contracting origin-centered ellipses.Comment: I changed the title and fixed some typos. To appear in Annales de l'Institut Henri Poincar\'e (C) Analyse Non Lin\'eair

C. elegans LIN-28 controls temporal cell fate progression by regulating LIN-46 expression via the 5\u27 UTR of lin-46 mRNA

Lin28/LIN-28 is a conserved RNA-binding protein that promotes proliferation and pluripotency and can be oncogenic in mammals. Mammalian Lin28 and C. elegans LIN-28 have been shown to inhibit biogenesis of the conserved cellular differentiation-promoting microRNA let-7 by directly binding to unprocessed let-7 transcripts. Lin28/LIN-28 also bind and regulate many mRNAs in diverse cell types. However, the determinants and consequences of LIN-28-mRNA interactions are not well understood. Here, we report that C. elegans LIN-28 represses the expression of LIN-46, a downstream protein in the heterochronic pathway. We find that lin-28 and sequences within the lin-46 5\u27 UTR are required to prevent LIN-46 expression at early larval stages. Moreover, we find that precocious LIN-46 expression caused by mutations in the lin-46 5\u27 UTR is sufficient to cause precocious heterochronic defects similar to those of lin-28(lf) animals. Thus, our findings demonstrate the biological importance of the regulation of individual target mRNAs by LIN-28

C. elegans LRP-2 functions in vulval precursor cell polarity

The C. elegans vulva is formed from divisions of three vulval precursor cells (VPCs) – P5.p, P6.p, and P7.p – arranged along the anteroposterior axis in the ventral epithelium (Sulston and Horvitz, 1977). Previous analyses show the orientation of P5.p and P7.p descendants is determined by the interaction of multiple Wnt signals. Specifically, in the absence of all Wnts, the VPCs display a randomized orientation, which is likely the default (Green et al., 2008; Minor et al. 2013). Two separate Wnts from the anchor cell, LIN-44 and MOM-2 acting through receptors LIN-17/Frizzled and LIN-18/Ryk, respectively, regulate P7.p orientation (Ferguson et al., 1987; Sternberg and Horvitz, 1988; Sawa et al., 1996; Inoue et al., 2004; Gleason et al., 2006). In the absence of these signals the orientation of the progeny of P7.p mimic those of P5.p and face toward the posterior of the worm, a phenotype referred to as posterior-reversed vulval lineage (P-Rvl). This posterior orientation is dependent on the instructive signal EGL-20, a Wnt expressed in the tail acting through CAM-1/ROR and VANG-1/Van Gogh, and is referred to as “ground polarity” (Green et al., 2008). Here we examine the role of a low-density lipoprotein receptor, lrp-2, and its role in controlling the orientation of P7.p daughter cells. To investigate this interaction double mutants were constructed with both alleles of lrp-2 and lin-17(n671) (Table 1). Much like cam-1(gm122) and vang-1(ok1142), both alleles of lrp-2 suppress the lin-17(n671) phenotype from 74 to approximately 50% P-Rvl leading us to hypothesize that lrp-2 functions in the same pathway as cam-1 and vang-1. Furthering this hypothesis we have shown that, like cam-1 and vang-1, lrp-2 controls the localization of SYS-1/b-catenin (Minor and Sternberg, 2019). To ensure that this phenotype was a result of loss of lrp-2 function as opposed to background effects we injected a fosmid (WRM0617cA02) containing the full-length sequence of lrp-2 and found that it does rescue the double mutant phenotype of lin-17(n671); lrp-2(gk272) from 55 to 73%. In order to better test this hypothesis a triple mutant was constructed between lin-17(n671), lrp-2(gk272), and cam-1(gm122) (Table 1). This triple mutant displays the same P-Rvl penetrance as both the lin-17(n671); lrp-2(gk272) and lin-17(n671); cam-1(gm122) double mutants confirming that lrp-2 functions in the same pathway as cam-1

C. elegans LRP-2 functions in vulval precursor cell polarity

The C. elegans vulva is formed from divisions of three vulval precursor cells (VPCs) – P5.p, P6.p, and P7.p – arranged along the anteroposterior axis in the ventral epithelium (Sulston and Horvitz, 1977). Previous analyses show the orientation of P5.p and P7.p descendants is determined by the interaction of multiple Wnt signals. Specifically, in the absence of all Wnts, the VPCs display a randomized orientation, which is likely the default (Green et al., 2008; Minor et al. 2013). Two separate Wnts from the anchor cell, LIN-44 and MOM-2 acting through receptors LIN-17/Frizzled and LIN-18/Ryk, respectively, regulate P7.p orientation (Ferguson et al., 1987; Sternberg and Horvitz, 1988; Sawa et al., 1996; Inoue et al., 2004; Gleason et al., 2006). In the absence of these signals the orientation of the progeny of P7.p mimic those of P5.p and face toward the posterior of the worm, a phenotype referred to as posterior-reversed vulval lineage (P-Rvl). This posterior orientation is dependent on the instructive signal EGL-20, a Wnt expressed in the tail acting through CAM-1/ROR and VANG-1/Van Gogh, and is referred to as “ground polarity” (Green et al., 2008). Here we examine the role of a low-density lipoprotein receptor, lrp-2, and its role in controlling the orientation of P7.p daughter cells. To investigate this interaction double mutants were constructed with both alleles of lrp-2 and lin-17(n671) (Table 1). Much like cam-1(gm122) and vang-1(ok1142), both alleles of lrp-2 suppress the lin-17(n671) phenotype from 74 to approximately 50% P-Rvl leading us to hypothesize that lrp-2 functions in the same pathway as cam-1 and vang-1. Furthering this hypothesis we have shown that, like cam-1 and vang-1, lrp-2 controls the localization of SYS-1/b-catenin (Minor and Sternberg, 2019). To ensure that this phenotype was a result of loss of lrp-2 function as opposed to background effects we injected a fosmid (WRM0617cA02) containing the full-length sequence of lrp-2 and found that it does rescue the double mutant phenotype of lin-17(n671); lrp-2(gk272) from 55 to 73%. In order to better test this hypothesis a triple mutant was constructed between lin-17(n671), lrp-2(gk272), and cam-1(gm122) (Table 1). This triple mutant displays the same P-Rvl penetrance as both the lin-17(n671); lrp-2(gk272) and lin-17(n671); cam-1(gm122) double mutants confirming that lrp-2 functions in the same pathway as cam-1

LRP-2 controls the localization of C. elegans SYS-1/beta-catenin

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