2026-10-14T07:24:35Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33989301 2026-09-24T17:49:30Z category_1 category_4 category_12 category_13 category_14 category_734 category_61 portal_5 item_type_3 month_year_09_2026

<p>Sequences of primers used in this study.</p> Penghui Song (6548540) Lijuan Ma (4335364) Dong Yan (356556) Biophysics Biochemistry Cell Biology Genetics Molecular Biology Biological Sciences not elsewhere classified Developmental Biology seq analysis indicates mutant germ cells gfp localizes predominantly exhibit multiple developmental div >< p abundant chemical modifications severe gametogenesis defects dependent splicing regulation mettl16 loss affects several model organisms mutants likely stem 6 </ sup drosophila mettl16 </ drosophila </ mettl16 </ behavioral defects alternative splicing mettl16 interacts methyltransferase mettl16 including mettl16 although mettl16 spermatid elongation small subset remains unknown pleiotropic phenotypes meiotic stages female mutants broad effect ), one <div><p>N⁶-methyladenosine (m⁶A), one of the most abundant chemical modifications on RNA, is installed by METTL3 and several other methyltransferases, including METTL16. Although METTL16 has been characterized in several model organisms, its function in <i>Drosophila</i> remains unknown. Here, we show that, unlike in mammals, <i>Drosophila Mettl16</i> mutants are viable but exhibit multiple developmental and behavioral defects. Both male and female mutants are sterile, with severe gametogenesis defects. <i>Mettl16</i> mutant germ cells can pass the mitotic and meiotic stages, but are defective in spermatid elongation and individualization. Mettl16-GFP localizes predominantly to the nucleus, and its absence does not impair global protein synthesis in wing disc epithelial cells. MeRIP-Seq analysis indicates that Mettl16 loss affects m⁶A on only a small subset of transcripts, in contrast to the broad effect of Mettl3. We further demonstrate that Mettl16 interacts with U6 snRNA and is required for its m⁶A modification. Accordingly, <i>Mettl16</i> mutants display widespread alterations in alternative splicing. Together, the pleiotropic phenotypes of <i>Mettl16</i> mutants likely stem from its role in m⁶A deposition and U6-dependent splicing regulation of specific target transcripts.</p></div> 2026-09-24T17:49:09Z Dataset Dataset 10.1371/journal.pgen.1012317.s016 https://figshare.com/articles/dataset/_p_Sequences_of_primers_used_in_this_study_p_/33989301 CC BY 4.0