Special Issue "Ciliate Genetics and Epigenetics"
Deadline for manuscript submissions: 31 March 2019
Ciliates have been well-established as model organisms to investigate genetics and epigenetics. These single cell eukaryotes have two types of nuclei: germline micro- and somatic macronuclei. Some of the first epigenetic phenomena were described in these organisms, and research over the last few decades has elucidated mechanisms that underlie these phenomena. Ciliates helped pioneer the current understanding of RNA interference, both for siRNA-mediated silencing and for small RNA-directed chromatin modification and DNA rearrangements, which provide cells a powerful tool to transmit epigenetic information to sexual progeny. Progress in our understanding of molecular mechanisms came from classical genetics studies and from genomics, post-genomics and the recent advances in epigenomics technologies.
This Special Issue provides an overview on the genetics and epigenetics in ciliates and their impacts on adaptation and evolution. We invite submissions for reviews, research articles, or short-communications reporting molecular genetics and epigenomics studies of ciliate research.
We will accept manuscripts starting in September until the deadline.
Prof. Dr. Martin Simon
Dr. Marcel Schulz
Prof. Dr. Douglas Chalker
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- RNA interference
- Non coding RNA
- Genome rearrangement
- Chromatin modification
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
1) Tentative Title: Loss of the gene localized in a fragile chromosome region leads to screwy phenotype in Paramecium tetraurelia
Tentative Abstract: The Spinning Top mutant of Paramecium tetraurelia strain 51 with a vivid phenotype has the micronuclear (MIC) deletion of a ~30-kb segment containing fifteen genes, which corresponds to the right end of scaffold 77 in the wild-type macronuclear (MAC) genome. The MAC deletion of the mutant parent is not maternally inherited in the cross to the wild type, as all F1 heterozygotes show a wild-type phenotype. We tested several candidate genes in the deleted locus by dsRNA-induced silencing, and identified a single gene responsible for the phenotype. This gene, which encodes a 566-aa glutamine-rich protein with two C2HC zinc fingers, was named Spade. Silencing of the Spade gene in vegetative cells leads to fast phenotype switch, and cells recover a wild-type phenotype after 5-6 divisions when dsRNA feeding is stopped. dsRNA feeding during autogamy results in variable MAC deletions and variable phenotypes in postautogamous progeny. The Spinning Top phenotype resembles the phenotypes of previously reported “screwy” mutants. We analyzed five different “screwy” mutants, and concluded that all of them lack the Spade gene and a number of neighboring genes, while the deletion length varies from 17,5 kb to 30 kb in different alleles. All MAC deletions were confirmed to be due to collinear MIC deletions, thus the respective MIC region is intrinsically unstable in the strain 51 genome.
Authors: Irina Nekrasova, Vera Nikitashina, Simran Bhullar, Deepankar P. Singh, Eric Meyer, Alexey Potekhin*
2) Tentative Title: Novel Role for Polycystin-2 (Pkd2) in P. tetraurelia as a Probable Mg2+ Channel Necessary for Mg2+ Induced Behavior
Tentative Abstract: Polycystin-2 (Pkd2), a non-selective cation channel, is a versatile human ciliopathy gene. Here, the location and activity of a proposed Pkd2 channel was explored using the ciliated organism, Paramecium tetraurelia. Using combinations of RNA interference, over-expression, and epitope-tagging, the role of the proposed Pkd2 channel was explored in Paramecium, which lacks most of the published interacting partners of Pkd2. Upon depletion of Pkd2, cells exhibited a phenotype similar to eccentric (XntA1), a Paramecium mutant lacking the inward Ca2+-dependent Mg2+ conductance. Further investigation showed both Pkd2 and XntA localize to the cilia and cell membrane, but do not require one another for trafficking. The XntA-myc protein co-immunoprecipitates Pkd2-FLAG, but not vice versa, suggesting two populations of Pkd2-FLAG, one of which interacts with XntA. Electrophysiology data showed that depletion and over-expression of Pkd2 led to smaller and larger depolarizations in Mg2+ solutions, respectively. Over-expression of Pkd2-FLAG in the XntA1 mutant caused slower swimming, supporting an increase in Mg2+ permeability, in agreement with the electrophysiology data. We propose that Pkd2 in P. tetraurelia collaborates with XntA for Mg2+-induced behavior. Our data suggest Pkd2 is sufficient and necessary for Mg2+ conductance, membrane permeability to Mg2+, and that Pkd2 is a Mg2+-permeable channel.
Authors: Megan S. Valentine*, Junji Yano, and Judith Van Houten