Lynch, S. C. | bioRxiv Science

bioRxiv2025

Two morphologically distinct formae speciales in Neonectria magnoliae differ in their virulence on Magnolia family hosts Liriodendron tulipifera and Magnolia fraseri

The family Nectriaceae includes numerous phytopathogenic fungal genera that cause canker diseases on both angiosperm and conifer hosts worldwide. Among these, Neonectria species are globally important canker pathogens of numerous hosts, but their roles in contributing to forest decline and mortality outside their role in beech bark disease and apple canker are largely understudied. In the U.S., Neonectria magnoliae causes perennial cankers on two native hosts in central Appalachia: Fraser magnolia (Magnolia fraseri) and tulip-poplar (Liriodendron tulipifera) and has been recently confirmed from non-native star magnolia (Magnolia stellata) in West Virginia. Both native hosts occur in the central Appalachian Mountains, but Fraser magnolia occurs mostly at higher elevations. Neonectria magnoliae was first described in 1943, yet its impact across the forested landscape remains unclear. To clarify host-specific differences across the contemporary range of Neonectria magnoliae, we used multi-locus phylogenetics, comparative pathogenicity / virulence assays, and morphological analyses to determine if N. magnoliae represents two cryptic species that specialize on tulip-poplar and magnolia, or if N. magnoliae has host-specific pathotypes. Our studies revealed two morphologically distinct formae speciales within N. magnoliae: 1) Neonectria magnoliae f. sp. liriodendri; strains originating from tulip-poplar with increased virulence on this host and lacking macroconidia production and 2) Neonectria magnoliae f. sp. magnoliae; strains originating from Fraser magnolia with increased virulence on this host and producing macroconidia readily in culture. Overall, the incidence of these two pathotypes indicates that neither pathogen alone poses serious risks to either host but adds to cumulative stresses that both tree species are experiencing in the face of global climate change.

microbiology↗

bioRxiv2023

Acyl-CoA thioesterase-2 facilitates beta-oxidation in glycolytic skeletal muscle in a lipid supply dependent manner

Acyl-Coenzyme A (acyl-CoA) thioesters are compartmentalized intermediates that participate in in multiple metabolic reactions within the mitochondrial matrix. The limited availability of free CoA (CoASH) in the matrix raises the question of how the local acyl-CoA concentration is regulated to prevent trapping of CoASH from overload of any specific substrate. Acyl-CoA thioesterase-2 (ACOT2) hydrolyzes long-chain acyl-CoAs to their constituent fatty acids and CoASH, and is the only mitochondrial matrix ACOT refractory to inhibition by CoASH. Thus, we reasoned that ACOT2 may constitutively regulate matrix acyl-CoA levels. Acot2 deletion in murine skeletal muscle (SM) resulted in acyl-CoA build-up when lipid supply and energy demands were modest. When energy demand and pyruvate availability were elevated, lack of ACOT2 activity promoted glucose oxidation. This preference for glucose over fatty acid oxidation was recapitulated in C2C12 myotubes with acute depletion of Acot2, and overt inhibition of {beta}-oxidation was demonstrated in isolated mitochondria from Acot2-depleted glycolytic SM. In mice fed a high fat diet, ACOT2 enabled the accretion of acyl-CoAs and ceramide derivatives in glycolytic SM, and this was associated with worse glucose homeostasis compared to when ACOT2 was absent. These observations suggest that ACOT2 supports CoASH availability to facilitate {beta}-oxidation in glycolytic SM when lipid supply is modest. However, when lipid supply is high, ACOT2 enables acyl-CoA and lipid accumulation, CoASH sequestration, and poor glucose homeostasis. Thus, ACOT2 regulates matrix acyl-CoA concentration in glycolytic muscle, and its impact depends on lipid supply.

biochemistry↗