Ariel - Volume 2 Number 2

Editors Delvyn C. Case, Jr. Paul M. Fernhoff News Editors Richard Bonanno Daniel B. Gould Ronald A. Hoffman Lay-Out Editor Carol Dolinskas Sports Editor James J. Nocon Contributing Editors MichaeI J. Blecker Lin Sey Edwards Jack Guralnik W. Cherry Light Features Editor Donald A. Bergman Stephen P. Flynn Business Manager Nick Grego Public Relations Robin A. Edward

Fate specification and tissue-specific cell cycle control of the <i>Caenorhabditis elegans</i> intestine

Coordination between cell fate specification and cell cycle control in multicellular organisms is essential to regulate cell numbers in tissues and organs during development, and its failure may lead to oncogenesis. In mammalian cells, as part of a general cell cycle checkpoint mechanism, the F-box protein β-transducin repeat-containing protein (β-TrCP) and the Skp1/Cul1/F-box complex control the periodic cell cycle fluctuations in abundance of the CDC25A and B phosphatases. Here, we find that the Caenorhabditis elegans β-TrCP orthologue LIN-23 regulates a progressive decline of CDC-25.1 abundance over several embryonic cell cycles and specifies cell number of one tissue, the embryonic intestine. The negative regulation of CDC-25.1 abundance by LIN-23 may be developmentally controlled because CDC-25.1 accumulates over time within the developing germline, where LIN-23 is also present. Concurrent with the destabilization of CDC-25.1, LIN-23 displays a spatially dynamic behavior in the embryo, periodically entering a nuclear compartment where CDC-25.1 is abundant

Controlling occupational cancers in Australia

Lin Fritschi, Renae C Fernandez, Deborah A Vallance, Terry J Slevin, Alison Reid, Timothy R Driscoll, Deborah C Glas

Resonance scattering at lyman-alpha by an atomic hydrogen cell

Hydrogen cell and ion chamber for obtaining photoelectric data on resonance scattering at lyman alpha lin

Structural Requirements for the Tissue-Specific and Tissue-General Functions of the Caenorhabditis elegans Epidermal Growth Factor LIN-3

Caenorhabditis elegans lin-3 encodes a homolog of the epidermal growth factor (EGF) family of growth factors. LIN-3 is the inductive signal for hermaphrodite vulval differentiation, and it is required for animal viability, hermaphrodite fertility, and the specification of anterior cell fates in the male B cell lineage. We describe the cloning of a lin-3 homolog from C. briggsae, sequence comparison of C. elegans lin-3 with C. briggsae lin-3, and the determination of molecular lesions in alleles of C. elegans lin-3, including three new alleles. We also analyzed the severity of phenotypes caused by the new and existing alleles of lin-3. Correlation of mutant phenotypes and their molecular lesions, as well as sequence comparison between two species, reveal that the EGF motif and the N-terminal portion of the cytoplasmic domain are important for the functions of LIN-3 in all tissues, while the C-terminal portion of the cytoplasmic domain is involved in the tissue-specific functions of lin-3. We discuss how the structure of lin-3 contributes to its functions in multiple developmental processes

The phylogenetic and geographic structure of Y-chromosome haplogroup R1a

none32siR1a-M420 is one of the most widely spread Y-chromosome haplogroups; however, its substructure within Europe and Asia has remained poorly characterized. Using a panel of 16 244 male subjects from 126 populations sampled across Eurasia, we identified 2923 R1a-M420 Y-chromosomes and analyzed them to a highly granular phylogeographic resolution. Whole Y-chromosome sequence analysis of eight R1a and five R1b individuals suggests a divergence time of ∼25 000 (95% CI: 21 300-29 000) years ago and a coalescence time within R1a-M417 of ∼5800 (95% CI: 4800-6800) years. The spatial frequency distributions of R1a sub-haplogroups conclusively indicate two major groups, one found primarily in Europe and the other confined to Central and South Asia. Beyond the major European versus Asian dichotomy, we describe several younger sub-haplogroups. Based on spatial distributions and diversity patterns within the R1a-M420 clade, particularly rare basal branches detected primarily within Iran and eastern Turkey, we conclude that the initial episodes of haplogroup R1a diversification likely occurred in the vicinity of present-day Iran.openUnderhill PA; Poznik GD; Rootsi S; Järve M; Lin AA; Wang J; Passarelli B; Kanbar J; Myres NM; King RJ; Di Cristofaro J; Sahakyan H; Behar DM; Kushniarevich A; Sarac J; Saric T; Rudan P; Pathak AK; Chaubey G; Grugni V; Semino O; Yepiskoposyan L; Bahmanimehr A; Farjadian S; Balanovsky O; Khusnutdinova EK; Herrera RJ; Chiaroni J; Bustamante CD; Quake SR; Kivisild T; Villems R.Underhill, Pa; Poznik, Gd; Rootsi, S; Järve, M; Lin, Aa; Wang, J; Passarelli, B; Kanbar, J; Myres, Nm; King, Rj; Di Cristofaro, J; Sahakyan, H; Behar, Dm; Kushniarevich, A; Sarac, J; Saric, T; Rudan, P; Pathak, Ak; Chaubey, G; Grugni, Viola; Semino, Ornella; Yepiskoposyan, L; Bahmanimehr, A; Farjadian, S; Balanovsky, O; Khusnutdinova, Ek; Herrera, Rj; Chiaroni, J; Bustamante, Cd; Quake, Sr; Kivisild, T; Villems, R

CACHD1: a new activity-modifying protein for voltage-gated calcium channels

Autocommentary to: Cottrell GS, Soubrane CH, Hounshell JA, Lin H, Owenson V, Rigby M, Cox PJ, Barker BS, Ottolini M, Ince S, Bauer, CC, Perez-Reyes E, Patel MK, Stevens EB, Stephens GJ (2018) CACHD1 is an 2-like protein that modulates CaV3 voltage-gated calcium channel activity J Neurosci 38:9186-9201

Carboxy-Terminal Truncation Activates glp-1 Protein to Specify Vulval Fates in Caenorhabditis elegans

The glp-1 and lin-12 genes encode homologous transmembrane proteins that may act as receptors for cell interactions during development. The glp-1 product is required for induction of germ-line proliferation and for embryogenesis. By contrast, lin-12 mediates somatic cell interactions, including those between the precursor cells that form the vulval hypodermis (VPCs). Here we analyse an unusual allele of glp-1, glp-1(q35), which displays a semidominant multivulva phenotype (Muv), as well as the typical recessive, loss-of-function Glp phenotypes (sterility and embryonic lethality). We find that the effects of glp-1(q35) on VPC development mimic those of dominant lin-12 mutations, even in the absence of lin-12 activity. The glp-1(q35) gene bears a nonsense mutation predicted to eliminate the 122 C-terminal amino acids, including a ProGluSerThr (PEST) sequence thought to destabilize proteins. We suggest that the carboxy terminus bears a negative regulatory domain which normally inactivates glp-1 in the VPCs. We propose that inappropriate glp-1(q35) activity can substitute for lin-12 to determine vulval fate, perhaps by driving the VPCs to proliferate

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