Analysis of m6A RNA methylation in Caenorhabditis elegans

Sendinc, Erdem; Valle-García, David; Jiao, Alan; Shi, Yang

doi:10.1038/s41421-020-00186-6

Cited by 25 publications

(20 citation statements)

References 17 publications

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“…The mouse RNA serves as an internal technical control because m 6 A sites are already mapped in this system (Wojtas et al, 2017). Compared with over 20,000 mouse peaks, we identified only 176 m 6 A peaks in the worm poly(A) + transcriptome (Figures S1B-S1D), which likely reflects the absence of the METTL3/METTL14 writer complex in worms (Sendinc et al, 2020;van Delft et al, 2017). Indeed, a motif analysis of the mouse peaks reveals the presence of the expected RRACH context (R = A and G; H = A, C, and U) used by the dominant mammalian METTL3/METTL14 writer (Figure 1D;Dominissini et al, 2012;Ke et al, 2015;Meyer et al, 2012), and this is absent in worms.…”

Section: Resultsmentioning

confidence: 92%

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

Mendel¹,

Delaney²,

Pandey³

et al. 2021

Cell

130

121

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Section: Resultsmentioning

confidence: 92%

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

Mendel¹,

Delaney²,

Pandey³

et al. 2021

Cell

130

121

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“…In addition, the m 6 A methyltransferase complex has also been studied in B. mori and C. elegans . In Bombyx , BmMETTL3 and BmMETTL14 have been identified as orthologs of METTL3 and METTL14 (Zhang et al, 2020 ), while in Caenorhabditis , F33A8.4 and C38D4.9 have been identified as the orthologs of ZC3H13 and METTL5 (Sendinc et al, 2020 ). They all function as methyltransferases.…”

Section: Discussionmentioning

confidence: 99%

“…Mutants of METTL3, METTL14, and YTHDC1 in Drosophila exhibit a common suite of molecular and phenotypic defects (Kan et al, 2017 ). However, no orthologs of METTL3 or METTL14 have been found in Caenorhabditis elegans , but F33A8.4 and C38D4.9 have been identified as orthologs of ZC3H13 and METTL5 (Sendinc et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

RNA N⁶‐methyladenosine modification suppresses replication of rice black streaked dwarf virus and is associated with virus persistence in its insect vector

Tian

Zhang

et al. 2021

Molecular Plant Pathology

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Rice black streaked dwarf virus (RBSDV) (species Rice black streaked dwarf virus, genus Fijivirus, family Reoviridae) is transmitted by the small brown planthopper (SBPH, Laodelphax striatellus) in a persistent propagative manner (Hibino, 1996). Since RBSDV was first identified in Japan in 1952(Kuribayashi & Shinkai, 1952, it has caused serious yield losses of rice and maize in East Asian countries, including several major outbreaks in China, Japan, and South Korea (Hibino, 1996;Wu et al., 2020). In nature, higher population densities of viruliferous SBPHs have largely contributed to RBSDV epidemics in rice and maize fields, especially at early stages of crop development (Chen & Zhang, 2005;Zhang, Wu, et al., 2021). At present, the best economical and effective method for managing RBSDV-induced diseases is controlling vector insects due to the lack of disease-resistant plant varieties. Therefore, understanding the transmission mechanism is crucial for accurate forecasting and disease control.The genome of RBSDV contains 10 double-stranded RNA (dsRNA) segments, S1 to S10, numbered in decreasing order of molecular weight (Milne et al., 2005). Most RBSDV genomic segments contain one open reading frame, but S5, S7, and S9 have two

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“…The strong conservation of these core factors suggests that the biochemical basis of N6 -adenosine methylation is common in eukaryotes and indeed, m 6 A occurs in the consensus site RR(m 6 A)CH (R=G/A, H=A/C/U), primarily in 3’-UTRs in animals (insects, mammals and fish), plants (maize and Arabidopsis) and fungi (yeast) that possess the canonical METTL3/METTL14 methyltransferase (Dominissini et al 2012; Meyer et al 2012; Schwartz et al 2013; Luo et al 2014; Lence et al 2016; Zhao et al 2017; Li et al 2019; Miao et al 2019; Parker et al 2020). Conversely, the characteristic motif and gene-body location is not detected in organisms that lack METTL3/METTL14 homologs, such as the nematode Caenorhabditis elegans (Sendinc et al 2020) and bacteria (Deng et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Principles of mRNA targeting via the Arabidopsis m⁶A-binding protein ECT2

Arribas-Hernández

Rennie

Köster

et al. 2021

Preprint

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Gene regulation dependent on N6-methyladenosine (m6A) in mRNA involves RNA-binding proteins that recognize m6A through a YTH domain. The Arabidopsis YTH-domain protein ECT2 is thought to influence mRNA 3′-end formation via binding to URU(m6A)Y sites, an unexpected conclusion given that ECT2 functions require its m6A binding activity, and that RR(m6A)CH is the m6A consensus site in all eukaryotes. Here, we apply the orthogonal techniques individual nucleotide-resolution UV-crosslinking and immunoprecipitation (iCLIP) and HyperTRIBE to define high-quality target sets of the YTH-domain proteins ECT2 and ECT3. The results show that in vivo, ECT2 does in fact bind to RR(m6A)CH. URUAY and other pyrimidine-rich motifs are enriched around, but not at m6A-sites, reflecting a preference for N6-adenosine methylation of RRACH islands in pyrimidine-rich regions. Such regions may also be implicated in ECT2-binding. In particular, a series of properties unique to the URUAY motif suggest that URUAY-type sequences act as sites of competition between unknown RNA-binding proteins and the intrinsically disordered region of ECT2. We also show that the abundance of many ECT2/3 mRNA targets is decreased in meristematic cells devoid of ECT2/3/4-activity. In contrast, loss of ECT2/3/4 activity has no effect on polyadenylation site usage in ECT2/3 targets, consistent with the exclusive cytoplasmic localization of ECT2 observed by super-resolution confocal microscopy. Our study reconciles conflicting results between genetic observations on N6-adenosine methylation and ECT2/3/4 function on the one side, and ECT2 target identification on the other, and point to regulation of cytoplasmic mRNA function, including abundance, as a mechanism of plant YTHDF action.

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Analysis of m6A RNA methylation in Caenorhabditis elegans

Cited by 25 publications

References 17 publications

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

RNA N⁶‐methyladenosine modification suppresses replication of rice black streaked dwarf virus and is associated with virus persistence in its insect vector

Principles of mRNA targeting via the Arabidopsis m⁶A-binding protein ECT2

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Analysis of m6A RNA methylation in Caenorhabditis elegans

Cited by 25 publications

References 17 publications

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing

RNA N6‐methyladenosine modification suppresses replication of rice black streaked dwarf virus and is associated with virus persistence in its insect vector

Principles of mRNA targeting via the Arabidopsis m6A-binding protein ECT2

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Product

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RNA N⁶‐methyladenosine modification suppresses replication of rice black streaked dwarf virus and is associated with virus persistence in its insect vector

Principles of mRNA targeting via the Arabidopsis m⁶A-binding protein ECT2