English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The catabolism of choline as a source of nitrogen in budding yeasts is thought to proceed via the intermediates trimethylamine, dimethylamine and methylamine before the release of ammonia. The present study investigated the utilisation of choline and its downstream intermediates as nitrogen sources in the yeast Scheffersomyces stipitis using a reverse genetics approach. Six genes (AMO1, AMO2, SFA1, FGH1, PICST_49761, PICST_63000) that have previously been predicted to be directly or indirectly involved in the catabolism of methylated amines were individually deleted. The growth of each deletion mutant was assayed on minimal media with methylamine, dimethylamine, trimethylamine or choline as the sole nitrogen source. The two amine oxidase-encoding genes AMO1 and AMO2 appeared to be functionally redundant for growth on methylated amines as both deletion mutants displayed growth on all nitrogen sources tested. However, deletion of AMO1 resulted in a pronounced growth lag on all four methylated amines while deletion of AMO2 only caused a growth lag when methylamine was the sole nitrogen source. The glutathione-dependent formaldehyde dehydrogenase-encoding gene SFA1 was found to be absolutely essential for growth on all methylated amines tested while deletion of the S-formylglutathione hydrolase gene FGH1 caused a pronounced growth lag on dimethylamine, trimethylamine and choline. The putative cytochrome P450 monooxygenase-encoding genes PICST_49761 and PICST_63000 were considered likely candidates for demethylation of di- and trimethylamine but produced no discernable phenotype on any of the tested nitrogen sources when deleted. This study revealed notable instances of genetic redundancies in the choline catabolic pathway, which are discussed.

Genetic redundancy in the catabolism of methylated amines in the yeast Scheffersomyces stipitis