scholarly journals Evidence for the Contribution of LTR Retrotransposons to C. elegans Gene Evolution

2003 ◽  
Vol 20 (11) ◽  
pp. 1925-1931 ◽  
Author(s):  
E. W. Ganko
2014 ◽  
Author(s):  
Dongying Gao ◽  
Yupeng Li ◽  
Brian Abernathy ◽  
Scott Jackson

Terminal-repeat retrotransposons in miniature (TRIMs) are structurally similar to long terminal repeat (LTR) retrotransposons except that they are extremely small and difficult to identify. Thus far, only a few TRIMs have been characterized in the euphyllophytes and the evolutionary and biological impacts and transposition mechanism of TRIMs are poorly understood. In this study, we combined de novo and homology-based methods to annotate TRIMs in 48 plant genome sequences, spanning land plants to algae. We found 156 TRIM families, 146 previously undescribed. Notably, we identified the first TRIMs in a lycophyte and non-vascular plants. The majority of the TRIM families were highly conserved and shared within and between plant families. Even though TRIMs contribute only a small fraction of any plant genome, they are enriched in or near genes and may play important roles in gene evolution. TRIMs were frequently organized into tandem arrays we called TA-TRIMs, another unique feature distinguishing them from LTR retrotransposons. Importantly, we identified putative autonomous retrotransposons that may mobilize specific TRIM elements and detected very recent transpositions of a TRIM in O. sativa. Overall, this comprehensive analysis of TRIMs across the entire plant kingdom provides insight into the evolution and conservation of TRIMs and the functional roles they may play in gene evolution.


Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 193-203
Author(s):  
Harmit S Malik ◽  
Thomas H Eickbush

Abstract Phylogenetic analyses of non-LTR retrotransposons suggest that all elements can be divided into 11 lineages. The 3 oldest lineages show target site specificity for unique locations in the genome and encode an endonuclease with an active site similar to certain restriction enzymes. The more “modern” non-LTR lineages possess an apurinic endonuclease-like domain and generally lack site specificity. The genome sequence of Caenorhabditis elegans reveals the presence of a non-LTR retrotransposon that resembles the older elements, in that it contains a single open reading frame with a carboxyl-terminal restriction-like endonuclease domain. Located near the N-terminal end of the ORF is a cysteine protease domain not found in any other non-LTR element. The N2 strain of C. elegans appears to contain only one full-length and several 5′ truncated copies of this element. The elements specifically insert in the Spliced leader-1 genes; hence the element has been named NeSL-1 (Nematode Spliced Leader-1). Phylogenetic analysis confirms that NeSL-1 branches very early in the non-LTR lineage and that it represents a 12th lineage of non-LTR elements. The target specificity of NeSL-1 for the spliced leader exons and the similarity of its structure to that of R2 elements leads to a simple model for its expression and retrotransposition.


2019 ◽  
Author(s):  
Sylvia E. J. Fischer ◽  
Gary Ruvkun

ABSTRACTEndogenous retroviruses and LTR retrotransposons are mobile genetic elements that are closely related to retroviruses. Desilenced endogenous retroviruses are associated with human autoimmune disorders and neurodegenerative diseases. C. elegans and related Caenorhabdites contain LTR retrotransposons and, as described here, numerous integrated viral genes including viral envelope genes that are part of LTR retrotransposons. We found that both LTR retrotransposons and endogenous viral elements are silenced by ADARs (adenosine deaminases acting on double-stranded RNA (dsRNA)) together with the endogenous RNAi factor ERI-6/7, a homolog of Mov10 helicase, a retrotransposon and retrovirus restriction factor in human. siRNAs corresponding to integrated viral genes and LTR retrotransposons, but not to DNA transposons, are dependent on the ADARs and ERI-6/7; on the contrary, siRNAs corresponding to palindromic repeats are increased in adar-eri mutants because of an antiviral RNAi response to dsRNA. Silencing of LTR retrotransposons is dependent on downstream RNAi factors and P granule components but is independent of the viral sensor DRH-1/RIG-I and the nuclear Argonaute NRDE-3. The activation of retrotransposons in the ADAR- and ERI-6/7/MOV10-defective mutant is associated with the induction of the Unfolded Protein Response (UPR), a common response to viral infection. The overlap between genes induced upon viral infection and infection with intracellular pathogens, and genes co-expressed with retrotransposons, suggests that there is a common response to different types of foreign elements that includes a response to proteotoxicity presumably caused by the burden of replicating pathogens and expressed retrotransposons.SIGNIFICANCESilencing of transposable elements and viruses is critical for the maintenance of genome integrity, cellular homeostasis and organismal health. Here we describe multiple factors that control different types of transposable elements, providing insight into how they are regulated. We also identify stress response pathways that are triggered upon mis-regulation of these transposable elements. The conservation of these factors and pathways in human suggests that our studies in C. elegans can provide general insight into the regulation of and response to transposable elements and viruses.


Gene ◽  
2004 ◽  
Vol 330 ◽  
pp. 61-66 ◽  
Author(s):  
Mika Zagrobelny ◽  
Daniel C. Jeffares ◽  
Peter Arctander

2021 ◽  
Author(s):  
Bo Yun Lee ◽  
Jun Kim ◽  
Junho Lee

Genes embed their evolutionary history in the form of various alleles. Presence absence variants (PAVs) are extreme cases of such alleles, where a gene present in one haplotype does not exist in another. Since PAVs may result from either birth or death of a gene, PAV genes and their alternative alleles, if available, can represent a basis for rapid intraspecific gene evolution. Here, we traced a possible evolution of PAV genes in the PD1074 and CB4856 C. elegans strains as well as their alternative alleles found in other 14 wild strains, using long-read sequencing technologies. We updated the CB4856 genome by filling 18 gaps and identified 50 novel genes and 7,460 novel isoforms from both strains. We verified 328 PAV genes, out of which 48 were C. elegans-specific. Among these possible newly-born genes, 13 had alternative alleles in other wild strains and, in particular, alternative alleles of three genes showed signatures active transposons. Alternative alleles of four other genes showed another type of signature reflected in accumulation of small insertions or deletions. Our results exemplify that research on gene evolution using both species-specific PAV genes and their alternative alleles is expected to provide new perspectives for how genes evolve.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
E. A. Baker ◽  
S. P. R. Gilbert ◽  
S. M. Shimeld ◽  
A. Woollard

AbstractBackgroundIt has been proposed that recently duplicated genes are more likely to be redundant with one another compared to ancient paralogues. The evolutionary logic underpinning this idea is simple, as the assumption is that recently derived paralogous genes are more similar in sequence compared to members of ancient gene families. We set out to test this idea by using molecular phylogenetics and exploiting the genetic tractability of the model nematode,Caenorhabditis elegans,in studying the nematode-specific family of Hedgehog-related genes, the Warthogs. Hedgehog is one of a handful of signal transduction pathways that underpins the development of bilaterian animals. While having lost abona fideHedgehog gene, most nematodes have evolved an expanded repertoire of Hedgehog-related genes, ten of which reside within the Warthog family.ResultsWe have characterised their evolutionary origin and their roles inC. elegansand found that these genes have adopted new functions in aspects of post-embryonic development, including left–right asymmetry and cell fate determination, akin to the functions of their vertebrate counterparts. Analysis of various double and triple mutants of the Warthog family reveals that more recently derived paralogues are not redundant with one another, while a pair of divergent Warthogs do display redundancy with respect to their function in cuticle biosynthesis.ConclusionsWe have shown that newer members of taxon-restricted gene families are not always functionally redundant despite their recent inception, whereas much older paralogues can be, which is considered paradoxical according to the current framework in gene evolution.


2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.


2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.


2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.


Author(s):  
Takaaki Hirotsu ◽  
Yu Hayashi ◽  
Ryo Iwata ◽  
Hirofumi Kunitomo ◽  
Eriko Kage-Nakadai ◽  
...  

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