Please use this identifier to cite or link to this item: http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/6341
Title: SUMOylation of Arginyl tRNA Synthetase Modulates the Drosophila Innate Immune Response
Authors: NAYAK, PRAJNA
KEJRIWAL, AARTI
RATNAPARKHI, GIRISH S.
Dept. of Biology
Keywords: MARS complex
NFkB
Signaling
CRISPR
Cas9
ArgRS
2021-OCT-WEEK3
TOC-OCT-2021
2021
Issue Date: Sep-2021
Publisher: Frontiers Media S.A.
Citation: Frontiers in Cell and Developmental Biology, 9, 695630.
Abstract: SUMO conjugation of a substrate protein can modify its activity, localization, interaction or function. A large number of SUMO targets in cells have been identified by Proteomics, but biological roles for SUMO conjugation for most targets remains elusive. The multi-aminoacyl tRNA synthetase complex (MARS) is a sensor and regulator of immune signaling. The proteins of this 1.2 MDa complex are targets of SUMO conjugation, in response to infection. Arginyl tRNA Synthetase (RRS), a member of the sub-complex II of MARS, is one such SUMO conjugation target. The sites for SUMO conjugation are Lys 147 and 383. Replacement of these residues by Arg (RRSK147R,K383R), creates a SUMO conjugation resistant variant (RRSSCR). Transgenic Drosophila lines for RRSWT and RRSSCR were generated by expressing these variants in a RRS loss of function (lof) animal, using the UAS-Gal4 system. The RRS-lof line was itself generated using CRISPR/Cas9 genome editing. Expression of both RRSWT and RRSSCR rescue the RRS-lof lethality. Adult animals expressing RRSWT and RRSSCR are compared and contrasted for their response to bacterial infection by gram positive M. luteus and gram negative Ecc15. We find that RRSSCR, when compared to RRSWT, shows modulation of the transcriptional response, as measured by quantitative 3′ mRNA sequencing. Our study uncovers a possible non-canonical role for SUMOylation of RRS, a member of the MARS complex, in host-defense.
URI: https://doi.org/10.3389/fcell.2021.695630
http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/6341
ISSN: 2296-634X
Appears in Collections:JOURNAL ARTICLES

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