Prathap N et al. (2023) Sci Rep "Prosopis juliflora hydrothermal synthesis of high fluorescent carbon dots and its antibacterial and bioimaging applications."

Karuppiah P, Prathap N, Venkatesan S, Shivakumar MS, Balla P, Ramasamy K, Periyasami G

[Sci Rep, 2023]

Carbon dots have stimulated the curiosity of biomedical researchers due to their unique properties, such as less toxicity and high biocompatibility. The synthesis of carbon dots for biomedical application is a core area in research. In the current research, an eco-friendly hydrothermal technique was employed to synthesize high fluorescent, plant-derived carbon dots from Prosopis juliflora leaves extract (PJ-CDs). The synthesized PJ-CDs were investigated by physicochemical evaluation instruments such as fluorescence spectroscopy, SEM, HR-TEM, EDX, XRD, FTIR, and UV-Vis. The UV-Vis absorption peaks obtained at 270 nm due to carbonyl functional groups shifts of n→π*. In addition, a quantum yield of 7.88 % is achieved. The synthesized PJ-CDs showing the presence of carious functional groups O-H, C-H, C=O, O-H, C-N and the obtained particles in spherical shape with an average size of 8 nm. The fluorescence PJ-CDs showed stability against various environmental factors such as a broad range of ionic strength and pH gradient. The antimicrobial activity of PJ-CDs was tested against a Staphylococcus aureus, and a Escherichia coli. The results suggest that the PJ-CDs could substantially inhibit the growth of Staphylococcus aureus. The findings also indicate that PJ-CDs are effective materials for bio-imaging in Caenorhabditis elegans and they can be also used for pharmaceutical applications.

Whittaker A et al. (2017) MicroPubl Biol "A new mutation with a polycystin phenotypic spectrum in Caenorhabditis elegans"

Schindelman G, Gharib S, Whittaker A, Sternberg PW

[MicroPubl Biol, 2017]

lov-1 and pkd-2, which encode the C. elegans orthologs of human polycystin-1 and -2, are necessary for three particular aspects of male mating behavior. In a screen for male mating defective mutants with similar spectrum of mating defects, we identified a mutation that apparently defines a new locus, lov-3. We isolated the sy682 mutation in an ethyl-methane sulphonate (EMS)-screen of Caenorhabditis elegans strain PS1395 [genotype: plg-1(e2001d); him-5(e1490)] for mutant males that do not mate efficiently and hence do not form plugs on hermaphrodites (Liu et al, 2017). sy682 is defective in the males response to contact with hermaphrodite and in vulval location (Table 1). The vulval location defect is failing to stop at the vulva. These two phenotypes are associated with lov-1 (Barr, 1999) and pkd-2 loss-of-function mutations (Barr et al. 2001; Whittaker et al., 2017). sy682 maps to the X chromosome and thus is distinct from lov-1 and pkd-2, so it defines a likely new locus, lov-3.

Maureen M Barr et al. (2001) International C. elegans Meeting "The C. elegans Autosomal Dominant Polycystic Kidney Disease Genes lov-1 and pkd-2 act in the same pathway"

Paul W Sternberg, Maureen M Barr

[International C. elegans Meeting, 2001]

Autosomal Dominant Polycystic Kidney Disease (ADPKD) strikes 1 in 1000 individuals, often resulting in end-stage renal failure. Mutations in either PKD1 or PKD2 account for 95% of all cases. Recently, polycystin-1 and polycystin-2 (encoded by PKD1 and PKD2, respectively) have been shown to form a cation channel in vitro (1). Here we show that the C. elegans homologues of PKD1 and PKD2, lov-1 and pkd-2 (2), act in the same pathway in vivo . Mutations in either lov-1 or pkd-2 result in identical male sensory behavioral defects. Furthermore, pkd-2; lov-1 double mutants are phenotypically indistinguishable from lov-1 and pkd-2 single mutants, indicating that lov-1 and pkd-2 act together. LOV-1 and PKD-2 protein colocalize to male-specific chemosensory neurons and concentrate in cilia. Consistent with a role in sensory signal transduction, basodendritic localization of PKD-2 is essential for function. In contrast to defects in the C. elegans Autosomal Recessive PKD gene osm-5 (3), the cilia of C. elegans ADPKD mutants are wild type as judged by electron microscopy. This system provides a genetically tractable model for determining molecular mechanisms underlying PKD. 1. Hanaoka, K. et al. Nature 408, 990-994 (2000). 2. Barr, M.M. & Sternberg, P.W. Nature 401, 386-9 (1999). 3. Qin, H., Rosenbaum, J.L. & Barr, M.M. Curr Biol 11. 457-461 (2001).

Wang, Juan et al. (2017) International Worm Meeting "Biogenesis and Function of Social Extracellular Vesicles (EVs)."

Barr, Maureen, Wang, Juan, Silva, Malan

[International Worm Meeting, 2017]

Extracellular vesicles are emerging as an important aspect of intercellular communication by delivering a parcel of proteins, lipids even nucleic acids to specific target cells over short or long distances (Maas 2017). A subset of C. elegans ciliated neurons release EVs to the environment and elicit changes in male behaviors in a cargo-dependent manner (Wang 2014, Silva 2017). Our studies raise many questions regarding these social communicating EV devices. Why is the cilium the donor site? What mechanisms control ciliary EV biogenesis? How are bioactive functions encoded within EVs? EV detection is a challenge and obstacle because of their small size (100nm). However, we possess the first and only system to visualize and monitor GFP-tagged EVs in living animals in real time. We are using several approaches to define the properties of an EV-releasing neuron (EVN) and to decipher the biology of ciliary-released EVs. To identify mechanisms regulating biogenesis, release, and function of ciliary EVs we took an unbiased transcriptome approach by isolating EVNs from adult worms and performing RNA-seq. We identified 335 significantly upregulated genes, of which 61 were validated by GFP reporters as expressed in EVNs (Wang 2015). By characterizing components of this EVN parts list, we discovered new components and pathways controlling EV biogenesis, EV shedding and retention in the cephalic lumen, and EV environmental release. We also identified cell-specific regulators of EVN ciliogenesis and are currently exploring mechanisms regulating EV cargo sorting. Our genetically tractable model can make inroads where other systems have not, and advance frontiers of EV knowledge where little is known. Maas, S. L. N., Breakefield, X. O., & Weaver, A. M. (2017). Trends in Cell Biology. Silva, M., Morsci, N., Nguyen, K. C. Q., Rizvi, A., Rongo, C., Hall, D. H., & Barr, M. M. (2017). Current Biology. Wang, J., Kaletsky, R., Silva, M., Williams, A., Haas, L. A., Androwski, R. J., Landis JN, Patrick C, Rashid A, Santiago-Martinez D, Gravato-Nobre M, Hodgkin J, Hall DH, Murphy CT, Barr, M. M. (2015).Current Biology. Wang, J., Silva, M., Haas, L. A., Morsci, N. S., Nguyen, K. C. Q., Hall, D. H., & Barr, M. M. (2014). Current Biology.

Calhoun, Adam et al. (2011) International Worm Meeting "Spatial memory in C. Elegans."

Chalasani, Sreekanth, Sharpee, Tatyana, Calhoun, Adam

[International Worm Meeting, 2011]

Worms are known to increase the frequency of turning and reversal events in response to removal of a food stimulus. This keeps the animal in a small area near the last observation of food. The increase in turning frequency is known to be regulated by dopamine and glutamate (Hills et al 2004). We have found that the search strategy is modified by the spatial pattern of food that is experienced. Worms adapt quickly to new food environments, learning spatial patterns on short timescales. The dopamine deficient cat-2 mutant is unable to learn different spatial patterns, suggesting that dopamine is required for spatial memory. References Hills T, Brockie PJ, Maricq AV (2004). Dopamine and glutamate control area-restricted search behavior in Caenorhabditis elegans. J Neurosci 24(5): 1217-1225.

Barr MM et al. (1999) Nature "A polycystic kidney-disease gene homologue required for male mating behaviour in C. elegans."

Barr MM, Sternberg PW

[Nature, 1999]

The stereotyped mating behaviour of the Caenorhabditis elegans male is made up of several substeps: response, backing, turning, vulva location, spicule insertion and sperm transfer. The complexity of this behaviour is reflected in the sexually dimorphic anatomy and nervous system. Behavioural functions have been assigned to most of the male-specific sensory neurons by means of cell ablations; for example, the hook sensory neurons HOA and HOB are specifically required for vulva location. We have investigated how sensory perception of the hermaphrodite by the C. elegans male controls mating behaviours. Here we identify a gene, lov-1 (for location of vulva), that is required for two male sensory behaviours: response and vulva location. lov-1 encodes a putative membrane protein with a mucin-like, serine-threonine-rich amino terminus followed by two blocks of homology to human polycystins, products of the autosomal dominant polycystic kidney-disease loci PKD1 and PKD2. LOV-1 is the closest C. elegans homologue of PKD1. lov-1 is expressed in adult males in sensory neurons of the rays, hook and head, which mediate response, vulva location, and potentially chemotaxis to hermaphrodites, respectively. PKD-2, the C. elegans homologue of PKD2, is localized to the same neurons as LOV-1, suggesting that they function in the same pathway.AD - Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena 91125, USA.FAU - Barr, M MAU - Barr MMFAU - Sternberg, P WAU - Sternberg PWLA - engPT - Journal ArticleCY - ENGLANDTA - NatureJID - 0410462RN - 0 (Helminth Proteins)RN - 0 (Membrane Proteins)RN - 0 (Proteins)RN - 0 (polycystic kidney disease 1 protein)SB - IM

Ansieau S et al. (2002) J Biol Chem "The conserved Mynd domain of BS69 binds cellular and oncoviral proteins through a common PXLXP motif."

Ansieau S, Leutz A

[J Biol Chem, 2002]

BS69 is a transcriptional co-repressor protein and a potential tumor suppressor that binds to the adenoviral oncoprotein E1A. We show that the C-terminal Mynd domain of BS69 (amino acids 516-561) or the closely related Mynd domains of the Caenorhabditis elegans proteins Bra-1 and Bra-2 bind not only to E1A but also to the Epstein-Barr virus EBNA2 oncoprotein and the Myc-related cellular protein MGA. Interaction depends on intact PXLXP motifs present in all three proteins. Moreover, viral proteins compete for binding of BS69 to MGA in a PXLXP-dependent fashion. Because deletions in E1A or EBNA2 that cover the PXLXP motifs are non-transforming, our observations suggest a role for BS69 in cell growth control that is reminiscent of abrogation of the Rb function by various oncoproteins.

Haas, Leonard A. et al. (2011) International Worm Meeting "The Effect of Hermaphrodite Sperm Status on C. elegans Sexual Attraction."

Haas, Leonard A., Barr, Maureen, Morsci, Natalia

[International Worm Meeting, 2011]

Sexual behaviors are modulated by numerous sensory signals. We use C. elegans to study how hermaphrodite-derived signals regulate male mating behavior. Male-specific genes lov-1 and pkd-2 are homologous to human autosomal dominant polycystic disease (ADPKD) genes. lov-1 and pkd-2 mutants are defective in multiple male sensory behaviors, including contact-based response (Barr and Sternberg 1999; Barr et al. 2001). Strikingly, lov-1 and pkd-2 males exhibited a threefold increase in response to sperm-depleted N2 or sperm-less fog-2 hermaphrodites. However, this improved response elicitation was decreased when fog-2 hermaphrodites were supplemented with male sperm. Wild-type males exposed to a mixture of sperm-depleted and self-sperm containing hermaphrodites also prefer sperm-depleted hermaphrodites. We conclude that hermaphrodite sperm status affects male mating behaviors via an unidentified ADPKD-independent pathway. We wanted to determine the nature of the signal that causes the increase in attractiveness to sperm-depleted hermaphrodites, using pkd-2 males as a sensitized background. We considered three possible sources that caused the increased attractiveness of sperm-depleted hermaphrodites: spermatogenesis, sperm activation, or the presence of fertilized oocytes. Through experiments with spe-19 and spe-38, we concluded that inactivated spermatids failed to inhibit hermaphrodite attractiveness; however, fertilization defective spermatozoa were capable of inhibiting hermaphrodite attractiveness. Although we do not know the molecular mechanism by which sperm signaling inhibits hermaphrodite mating cue, we show that it is triggered during or after sperm activation. We conclude that the reproductive state of the hermaphrodite impacts male behavior and mate choice. We are currently testing the different aspects of sperm activation for its effect on hermaphrodite attractiveness.

Emmons SW et al. (1999) Nature "Signal transduction. Mating, channels and kidney cysts."

Somlo S, Emmons SW

[Nature, 1999]

Advances in human genetics have meant that the genes mutated in human diseases can be identified exclusively by their location in the genome. But how do we work out the cellular functions of the associated protein products? Reports on pages 383 and 386 of this issue begin to address this problem for two proteins - polycystin-1 (PKD1) and polycystin-2 (PKD2) - that are defective in human kidney disease. From their studies of the nematode worm Caenorhabditis elegans, Barr and Sternberg present evidence that homologues of the polycystins act together in a signal-transduction pathway in sensory neurons. Chen et al., by contrast, have used an oocyte-expression system in the from Xenopus laevis to show that a homologue of PKD2 is associated with the activity of a cation channel. These results support the hypothesis that polycystin-related proteins belong to a hitherto unknown class of signal-transduction molecules.

Sengupta P et al. (2014) Traffic "New insights into an old organelle: meeting report on biology of cilia and flagella."

Barr MM, Sengupta P

[Traffic, 2014]

The rising interest of the scientific community in cilia biology was evident from the fact that registration for the third FASEB conference on 'The Biology of Cilia and Flagella' closed out before the early bird deadline. Cilia and flagella are organelles of profound medical importance; defects in their structure or function result in a plethora of human diseases called ciliopathies. 240 clinicians and basic scientists from around the world gathered from 23 June 2013 to 28 June 2013 at Sheraton at the Falls, Niagara Falls, NY to present and discuss their research on this intensely studied subcellular structure. The meeting was organized by Gregory Pazour (University of Massachusetts Medical School), Bradley Yoder (University of Alabama-Birmingham), and Maureen Barr (Rutgers University) and was sponsored by the Federation of American Societies for Experimental Biology (FASEB). Here, we report highlights, points of discussion, and emerging themes from this exciting meeting.