Salome-Correa, Jose et al. (2021) International Worm Meeting "Genomic landscape of the obligately outcrossing Caenorhabditis becei"

Salome-Correa, Jose, Noble, Luke, Sloat, Solomon, Rockman, Matthew

[International Worm Meeting, 2021]

Breeding systems determine the way genes are transmitted to the next generation, consequently driving genetic variation and genome evolution. Breeding systems may also play a role in the activity and prevalence of transposable elements. Selfing should increase the selection efficacy against TEs as a result of high homozygosity, with the majority of TEs present having reached fixation through genetic drift. Conversely, outcrossing should facilitate the spread of TE insertions throughout populations, and result in a higher number of moderately deleterious mutations. In the Caenorhabditis group Elegans, there doesn't appear to be a clear pattern of TE dynamics across partially-selfing species and obligately outcrossing species. Most species in the Elegans group, appear to have chromosomal heterogeneity in repeat density, with chromosome arms being more repeat rich, and gene poor, than the centers. This association is not always consistent, as is the case for the outcrossing species C. inopinata and C. bovis, where some, but not all, repeat types have a more uniform distribution across the chromosome, with little divergence between copies, which may indicate recent TE activity. It is currently unknown whether these observations are also found across species from the obligately outcrossing Caenorhabditis group Japonica. Here we present the first chromosome-scale assembly for a species belonging to the Japonica group, Caenorhabditis becei. This high-quality assembly was generated from PacBio long read data, Hi-C data, and a genetic map of an advanced intercross panel. The gene annotation for this genome was generated using Iso-Seq data and RNA-seq data from C. becei, as well as orthologous protein-coding and protein sequences from other Caenorhabditis species. We then characterized features such as synteny to other Caenorhabditis species, genome size, recombination rate domain structure, gene content, orthology, and distribution. We created a classified library of repetitive elements identified through de novo approaches. We generated TE annotations for the C. becei genome, and we reveal the patterns of repeat density, prevalence, distribution, and divergence.

Fassnacht, N. et al. (2019) International Worm Meeting "Chromatin remodeling mediates repair of DNA damage in C. elegans germ cells."

Peruffo , A., Fassnacht, N., Checchi, P.

[International Worm Meeting, 2019]

Chromatin remodeling proteins are required for multiple aspects of DNA repair. This is particularly important in germ cells, wherein defective repair affects gamete quality. This in turn leads to infertility, miscarriage, and chromosomal disorders. Previously, we discovered a role for the nucleosome remodeling and deacetylase (NuRD) chromatin remodeling complex in the repair of programmed DNA lesions. Loss of the catalytic component of NuRD, known as the Mi2 complex, disrupts repair of meiotic DSBs1. Here we investigated the role of the Mi2 component LET-418 in response to several forms of exogenous DNA damage. We assessed embryonic viability in response to several mutagens including nitrogen mustard and cisplatin, which cause inter- and/or intra-strand crosslinks (ICLs), a byproduct of replication errors. Our data reveal reduced embryonic viability in a let-418 loss-of-function mutant when mitotically dividing germ cells are exposed to these agents. This is consistent with previous findings that Mi2 has a role in the repair of double-stranded breaks, which can be formed from ICLs. We are currently assessing the molecular nature as to how LET-418 responds to ICLs and other types of DNA lesions, such as those caused by hydroxyurea and UVC. Overall, our findings support a role of Mi2 in maintaining genomic stability in multiple contexts. 1Turcotte, C.A., Sloat, S.A., Rigothi, J.A, Rosenkranse, E., Northrup, A., Andrews, N.P., and Checchi, P.M. (2018). Maintenance of genome integrity by Mi2 homologs CHD-3 and LET-418 in Caenorhabditis elegans. Genetics. 208:1-17.

Bennett, Heather L et al. (2011) International Worm Meeting "A role for heterochronic genes in regulating C.elegans quiescence."

Corkins, Mark E, Anderson, Edward, Singh, Komudi, Hart, Anne C, Bennett, Heather L

[International Worm Meeting, 2011]

Sleep is an essential biological process that is regulated by circadian rhythms, homeostatic regulation and arousal threshold. The nematode Caenorhabitdis elegans undergoes a sleep-like state called quiescence that accompanies each larval molt (Raizen et al., 2008). Many pathways regulate larval development, including heterochronic genes and the Notch signaling pathway. Heterochronic genes control timing of cell differentiation and molting of larval cuticle. In Drosophila, circadian rhythm proteins cycle to regulate sleep behavior. In C.elegans, circadian rhythm homologs in the heterochronic pathway regulate the fusion of hypodermal seam cells during late development (Jeon et al., 1999, Banerjee et al., 2005). Recently, a temporal role in C. elegans molting was suggested for the Notch signaling pathway. Gain of function alleles of a Notch receptor gene, lin-12, result in precocious cell fate changes (Solomon et al., 2007). We have found that Notch also plays a role in the regulation of quiescence. Increased or decreased Notch signaling results in increased quiescence and altered arousal thresholds during the last larval stage (L4) to adult (A) transition (Singh et al., in press). However, the connection between circadian rhythm homologs, heterochronic genes, and Notch in the regulation of quiescence remains unclear. We are assessing gain and loss of function alleles of heterochronic genes acting in the L4/A transition to determine if they play a role in regulating quiescence. Demonstrating a genetic interaction between heterochronic genes, circadian rhythm proteins, and the Notch signaling pathway will be the first step in delineating mechanisms that coordinate cell fate and behavioral changes during development.