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Remus, R.

Publications and source records attributed to Remus, R..

2 recordsLinked to original sources

Age-dependent differential iron deficiency responses of rosette leaves during reproductive stages in Arabidopsis thaliana

Iron (Fe) is essential for plant development throughout the life cycle. Rosette leaves are responsive to Fe supply in Arabidopsis thaliana. Little is known about the dynamics of Fe deficiency (-Fe) responses of rosette leaves during the reproductive stages. We studied the dynamics of Fe-dependent responses at four consecutive reproductive stages (rosette, bolting, flowering, mature silique stages, hereby named RS, BS, FS, MS). We examined the growth of rosette leaves, elemental contents and gene expression patterns of Fe homeostasis genes belonging to differently regulated groups. We determined individual leaf sizes during seven days of +Fe and -Fe treatment at the RS. Young leaves responded to -Fe with growth inhibition and yellowing. Old and young leaves differed in gene expression patterns and elemental contents. Differences were noted between the early and late reproductive stages (primarily RS and BS versus MS) and correlations between ionomic contents and gene expression were detected. All leaves had induced Fe recycling genes at -Fe. Our findings highlight a developmental stage-dependent modulation of +Fe and -Fe responses in leaves. We discuss possible leaf signaling mechanisms accounting for the distinct responses between old and young leaves. This insight is informative to strengthen our understanding on plant iron management. Highlight/ One-sentence summaryThis study explores reproductive stage-dependent responses of rosette leaves to iron availability, revealing distinct growth, elemental contents, and gene expression patterns between young and old leaves and stages.

plant biology↗

High-resolution respirometry reveals altered mammalian tissue ketone body oxidation in different cardiometabolic diseases

Background and aimsReduced mitochondrial function has been implicated in metabolic disorders like type 2 diabetes (T2D), obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD), which are tightly linked to insulin resistance and impaired metabolic flexibility. However, the contribution of the ketone bodies (KBs) {beta}-hydroxybutyrate (HBA) and acetoacetate (ACA) as substrates for mitochondrial oxidative phosphorylation (OXPHOS) in these insulin resistant states remains unclear. MethodsTargeted high-resolution respirometry protocols were applied to detect the differential contribution of HBA and ACA to OXPHOS capacity in heart, skeletal muscle, kidney, and liver of distinct human and mouse cohorts with T2D, obesity, and MASLD. ResultsIn humans with T2D, KB-driven mitochondrial OXPHOS capacity was [~]30% lower in the heart (p<0.05) and skeletal muscle (p<0.05) compared to non-diabetic controls. The relative contribution of KB to maximal OXPHOS capacity in T2D was also lower in both the heart ([~]25%, p<0.05) and skeletal muscle ([~]50%, p<0.05). Similarly, in kidney cortex from high-fat diet-induced obese mice, both the absolute and relative contribution of KB to OXPHOS capacity was [~]15% lower (p<0.05). Finally, hepatic HBA-driven mitochondrial OXPHOS capacity was 29% lower (p<0.05) in obese humans with MASLD compared to humans without MASLD. ConclusionsMitochondrial KB-driven OXPHOS capacity is impaired in insulin resistant states in various organs in absolute and relative terms, likely reflecting impaired mitochondrial metabolic flexibility. Our data suggest that KB respirometry can provide a sensitive readout of impaired mitochondrial function in diabetes, obesity, and MASLD.

cell biology↗