Year: 2021
Type: preprint
Abstract: ABSTRACT Neurospora Sk-2 is a complex meiotic drive element that is transmitted to offspring through sexual reproduction in a biased manner. Sk-2 ’s transmission mechanism involves spore killing, and recent evidence has demonstrated that its spore killing mechanism is mediated by a gene called rfk-1 . The native rfk-1 sequence, referred to as rfk-1 + , encodes an early UAG stop codon and a late UAA stop codon. When translation stops at the early stop codon, a 102 amino acid protein called RFK-1A is produced, and when translation stops at the late stop codon, a 130 amino acid protein called RFK-1B is produced. We show that expression of RFK-1B occurs when the early stop codon undergoes adenosine-to-inosine (A-to-I) mRNA editing (UAG is edited to UIG), and that this editing event is required for spore killing. We also show that RFK-1B, but not RFK-1A, acts as a poison when it is ectopically expressed within the vegetative tissue of a non- Sk-2 strain. Furthermore, we show that RFK-1B toxicity can be neutralized in vegetative tissue by co-expressing RSK Sk-2 , which is presumed to be Sk-2 ’s antidote protein. Finally, we show that rfk-1 + ’s first intron, or a truncated version of this intron, when present, improves phenotypic expression of RFK-1B in vegetative tissue. Overall, our results demonstrate that Sk-2 uses A-to-I mRNA editing to control when its killer protein (poison) is produced, and that the primary killing and resistance functions of Sk-2 can be established within a non- Sk-2 strain by the ectopic expression of only two genes.
Authors: Shahriar Mahmud, Thomas M. Hammond, Nicholas A. Rhoades
Institution: Illinois State University
Language: English
Topic: RNA regulation and disease
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Funder: National Science Foundation
OpenAlex ID: W3115470310