Energy cost of physical activities in growing broilers.

1. The time-energy budget method estimates the energy used for physical activity (PA) by integrating behaviour PA patterns with energy cost for specific PAs. Nevertheless, information about individual energy cost by type of PA are not available and so this study estimated the energy cost of PA for growing broilers.2. An indirect calorimetry system for single birds was constructed to measure the variation in the rate of O2 consumption (V˙O2, L/min) and rate of CO2 production (V˙CO2, L/min) produced by these PAs.3. A total of five birds were used in a replicated trial where their body weight (BW) ranged from 1.5 to 2.5 kg to measure the increase in heat production (HP) above resting levels as a result of PA. The procedure in the chamber was divided into five steps: (1) initial baselining, (2) resting metabolic rate, (3) PA such as feeding, drinking and other standing activities, (4) removal of gas exchange produced in step 3, and (5) final baselining. The PA was recorded using a video camera fixed at the chamber's top (and outside).4. The area under V˙CO2 and V˙O2 curves was used to calculate the CO2 production (vCO2, L) and O2 consumption (vO2, L). Then, the HP (cal/kg-0.75) was calculated according to the Brouwer equation. Two observers analysed the video records to estimate the time spent for each PA (seconds and frequency).5. To calculate the energetic coefficients, the HP was regressed with the function of time spent to perform each PA allowing to estimate the energy cost for eating, drinking and stand activities, which were 0.607, 0.352 and 0.938 cal/kg-0.75/s, respectively.

DNA Polymerase Beta Participates in Mitochondrial DNA Repair.

We have detected DNA polymerase beta (Polß), known as a key nuclear base excision repair (BER) protein, in mitochondrial protein extracts derived from mammalian tissue and cells. Manipulation of the N-terminal sequence affected the amount of Polß in the mitochondria. Using Polß fragments, mitochondrion-specific protein partners were identified, with the interactors functioning mainly in DNA maintenance and mitochondrial import. Of particular interest was the identification of the proteins TWINKLE, SSBP1, and TFAM, all of which are mitochondrion-specific DNA effectors and are known to function in the nucleoid. Polß directly interacted functionally with the mitochondrial helicase TWINKLE. Human kidney cells with Polß knockout (KO) had higher endogenous mitochondrial DNA (mtDNA) damage. Mitochondrial extracts derived from heterozygous Polß mouse tissue and KO cells had lower nucleotide incorporation activity. Mouse-derived Polß null fibroblasts had severely affected metabolic parameters. Indeed, gene knockout of Polß caused mitochondrial dysfunction, including reduced membrane potential and mitochondrial content. We show that Polß is a mitochondrial polymerase involved in mtDNA maintenance and is required for mitochondrial homeostasis.