Brendan James Battersby

Rapid plastid isolation reveals the chloroplast proteome and structures of the chlororibosome large subunit and RuBisCO in Marchantia polymorpha

This study isolates plastids from Marchantia polymorpha and determines their proteome and high-resolution structures of chlororibosome and RuBisCO, revealing structural conservation and functional insights.

Structure determination and dual targeting of a plant TACO1 identifies its ancient role as an organelle translation regulator

The paper identifies and structures MpTACO1, a dual-targeted protein in plants, showing its role in enhancing translation of mitochondrial and plastid-encoded proteins.

Intrinsic errors in mitochondrial translation trigger a decline in cell fitness.

This study shows that errors in mitochondrial translation cause cellular stress and metabolic changes linked to disease and aging, independent of oxidative phosphorylation.

DDHD2 provides a critical flux of saturated fatty acids to support neuronal energy demands

The paper shows that DDHD2-generated saturated fatty acids are essential for neuronal energy production and synaptic function.

Supernumerary proteins of the human mitochondrial ribosomal small subunit are integral for assembly and translation

The paper investigates the functional roles of 14 unique human mitochondrial ribosomal proteins in the small subunit, showing their essentiality in assembly and translation, with a redox-regulated role for mS37.

Translation of MT-ATP6 pathogenic variants reveals distinct regulatory consequencesfrom the co-translational quality control of mitochondrial protein synthesis.

The paper investigates how pathogenic variants in MT-ATP6 affect mitochondrial protein synthesis quality control and reveals distinct regulatory consequences on mitochondrial gene expression.

RNA nucleotide repeats induce mitochondrial dysfunction and the ribosome associated quality control

This study shows that RNA nucleotide repeats cause mitochondrial dysfunction and ribosome-associated quality control issues in C. elegans, with Coenzyme Q supplementation rescuing the defects.

Mice harboring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity.

This study creates a new mouse model with a patient-derived SCA28 mutation and shows it leads to late-onset ataxia and mitochondrial dysfunction.