Copley RR et al. (2004) Evol Dev "Systematic searches for molecular synapomorphies in model metazoan genomes give some support for Ecdysozoa after accounting for the idosyncrasies of Caenorhabditis elegans."

Telford MJ, Aloy P, Russell RB, Copley RR

[Evol Dev, 2004]

There has been broad acceptance among evolutionary biologists of the Ecdysozoa hypothesis that, based principally on molecular phylogenetic studies of small and large subunit ribosomal RNA sequences, postulates a close relationship between molting taxa such as arthropods and nematodes. On the other hand, recent studies of as many as 100 additional genes do not support the Ecdysozoa hypothesis and instead favor the older Coelomata hypothesis that groups the coelomate arthropods with the coelomate vertebrates to the exclusion of the nematodes. Here, exploiting completely sequenced genomes, we examined this question using cladistic analyses of the phylogenetic distribution of 1712 orthologous genes and 2906 protein domain combinations; we found stronger support for the Coelomata hypothesis than for the Ecdysozoa hypothesis. However, although arrived at by considering very large data sets, we show that this conclusion is unreliable, biased toward grouping arthropods with chordates by systematic high rate of character loss in the nematode. When we addressed this problem, we found slightly more support for Ecdysozoa than for Coelomata. Our identification of this systematic bias even when using entire genomes has important implications for future phylogenetic studies. We conclude that the results from the intensively sampled ribosomal RNA genes supporting the Ecdysozoa hypothesis provide the most credible current estimates of metazoan phylogeny.

Bichai F et al. (2009) Water Res "Protection against UV disinfection of E. coli bacteria and B. subtilis spores ingested by C. elegans nematodes."

Barbeau B, Bichai F, Payment P

[Water Res, 2009]

Nematodes, which occur abundantly in granular media filters of drinking water treatment plants and in distribution systems, can ingest and transport pathogenic bacteria and provide them protection against chemical disinfectants. However, protection against UV disinfection had not been investigated to date. In this study, Caenorhabditis elegans nematodes (wild-type strain N2) were allowed to feed on Escherichia coli OP50 and Bacillus subtilis spores before being exposed to 5 and 40 mJ/cm(2) UV fluences, using a collimated beam apparatus (LP, 254 nm). Sonication (15 W, 60s) was used to extract bacteria from nematode guts following UV exposure in order to assess the amount of ingested bacteria that resisted the UV treatment using a standard culture method. Bacteria located inside the gut of C. elegans were shown to benefit from a significant protection against UV. Approximately 15% of the applied UV fluence of 40 mJ/cm(2) (as typically used in WTP) was found to reach the bacteria located inside nematode guts based on the inactivation of recovered bacteria (2.7 log reduction of E. coli bacteria and 0.7 log reduction of B. subtilis spores at 40 mJ/cm(2)). To our knowledge, this study is the first demonstration of the protection effect of bacterial internalization by higher organisms against UV treatment, using the specific case of E. coli and B. subtilis spores ingested by C. elegans.

Wang H et al. (2018) NPJ Aging Mech Dis "A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans."

Telford MJ, Wang H, Gilliat AF, Girstmair J, Zhang Z, Galimov ER, Hellberg J, Dolphin CT, Ren Z, Gems D, Zhao Y, Benedetto A, Athigapanich T, Ezcurra M

[NPJ Aging Mech Dis, 2018]

A long-standing belief is that aging (senescence) is the result of stochastic damage accumulation. Alternatively, senescent pathology may also result from late-life, wild-type gene action (i.e., antagonistic pleiotropy, as argued by Williams) leading to non-adaptive run-on of developmental programs (or <i>quasi-programs</i>) (as suggested more recently by Blagosklonny). In this study, we use existing and new data to show how uterine tumors, a prominent form of senescent pathology in the nematode <i>Caenorhabditis elegans</i>, likely result from quasi-programs. Such tumors develop from unfertilized oocytes which enter the uterus and become hypertrophic and replete with endoreduplicated chromatin masses. Tumor formation begins with ovulation of unfertilized oocytes immediately after exhaustion of sperm stocks. We show that the timing of this transition between program and quasi-program (i.e., the onset of senescence), and the onset of tumor formation, depends upon the timing of sperm depletion. We identify homology between uterine tumors and mammalian ovarian teratomas, which both develop from oocytes that fail to mature after meiosis I. In teratomas, futile activation of developmental programs leads to the formation of differentiated structures within the tumor. We report that older uterine tumors express markers of later embryogenesis, consistent with teratoma-like activation of developmental programs. We also present evidence of coupling of distal gonad atrophy to oocyte hypertrophy. This study shows how the Williams Blagosklonny model can provide a mechanistic explanation of this component of <i>C. elegans</i> aging. It also suggests etiological similarity between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

Gong W et al. (2021) Cell Syst "Benchmarked approaches for reconstruction of invitro cell lineages and in silico models of C. elegans and M. musculus developmental trees."

Garry DJ, Guan Y, Shang X, Mason M, Shapiro E, Raz O, Telford MJ, Rennert P, Yu T, Chow KK, Shendure J, Srinivasan R, Granados AA, Zhang H, Rao A, Prusokas A, Elowitz MB, Saipradeep VG, Chung V, Khodaverdian A, Jones MG, Meyer P, Gong W, Wang R, Joseph T, Hu J, Retkute R, Yosef N, Kwak IY, Liu Z, Peng J, Rao S, Han L, Sivadasan N, Zhang R, Salvador-Martinez I

[Cell Syst, 2021]

The recent advent of CRISPR and other molecular tools enabled the reconstruction of cell lineages based on induced DNA mutations and promises to solve the ones of more complex organisms. To date, no lineage reconstruction algorithms have been rigorously examined for their performance and robustness across dataset types and number of cells. To benchmark such methods, we decided to organize a DREAM challenge using invitro experimental intMEMOIR recordings and in silico data for a C.elegans lineage tree of about 1,000 cells and a Mus musculus tree of 10,000 cells. Some of the 22 approaches submitted had excellent performance, but structural features of the trees prevented optimal reconstructions. Using smaller sub-trees as training sets proved to be a good approach for tuning algorithms to reconstruct larger trees. The simulation and reconstruction methods here generated delineate a potential way forward for solving larger cell lineage trees such as in mouse.