Effects of elevated CO_2, temperatue and nitrogen supply on growth quality and photosynthesis of sugar beet (Beta vulgaris L.)

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Response of sugar beet (Beta vulgaris L.) yield and biochemical composition to elevated CO2 and temperature at two nitrogen applications

Effects on sugar beet (Beta vulgaris L.) of current and elevated CO2 and temperature alone and in combination and their interactions with abundant and deficient nitrogen supply (HN and LN, respectively) have been studied in three experiments in 1993, 1994 and 1995. Averaged over all experiments, elevated CO2 (600 mu mol mol(-1) in 1993 and 700 mu mol mol-l in 1994 and 1995) increased total dry mass at final harvest by 21% (95% confidence interval (CI) = 21, 22) and 11% (CI = 6, 15) and root dry mass by 26% (CI = 19, 32) and 12% (CI = 6, 18) for HN and LN plants, respectively. Warmer temperature decreased total dry mass by 11% (CI = - 15, - 7) and 9% (CI = - 15, - 5) and root dry mass by 7% (CI = - 12, - 2) and 7% (CI = - 10, 0) for HN and LN plants, respectively. There was no significant interaction between temperature and CO2 on total or root dry mass. Neither elevated CO2 nor temperature significantly affected sucrose concentration per unit root dry mass. Concentrations of glycinebetaine and of amino acids, measured as alpha-amino-N, decreased in elevated CO2 in both N applications; glycinebetaine by 13% (CI = - 21, - 5) and 16% (CI = - 24, - 8) and alpha-amino-N by 24% (CI = - 36, - 11) and 16% (CI = - 26, - 5) for HN and LN, respectively. Warmer temperature increased alpha-amino-N, by 76% (CI = 50, 107) for HN and 21% (CI = 7, 36) for LN plants, but not glycinebetaine

Genome-wide RNA polymerase stalling shapes the transcriptome during aging

In aging mouse livers, 40% of elongating RNA polymerases are stalled, biasing transcriptional output dependent on gene length. This transcriptional stress appears to be caused by endogenous DNA damage.Gene expression profiling has identified numerous processes altered in aging, but how these changes arise is largely unknown. Here we combined nascent RNA sequencing and RNA polymerase II chromatin immunoprecipitation followed by sequencing to elucidate the underlying mechanisms triggering gene expression changes in wild-type aged mice. We found that in 2-year-old liver, 40% of elongating RNA polymerases are stalled, lowering productive transcription and skewing transcriptional output in a gene-length-dependent fashion. We demonstrate that this transcriptional stress is caused by endogenous DNA damage and explains the majority of gene expression changes in aging in most mainly postmitotic organs, specifically affecting aging hallmark pathways such as nutrient sensing, autophagy, proteostasis, energy metabolism, immune function and cellular stress resilience. Age-related transcriptional stress is evolutionary conserved from nematodes to humans. Thus, accumulation of stochastic endogenous DNA damage during aging deteriorates basal transcription, which establishes the age-related transcriptome and causes dysfunction of key aging hallmark pathways, disclosing how DNA damage functionally underlies major aspects of normal aging

Genome-wide RNA polymerase stalling shapes the transcriptome during aging

Gene expression profiling has identified numerous processes altered in aging, but how these changes arise is largely unknown. Here we combined nascent RNA sequencing and RNA polymerase II chromatin immunoprecipitation followed by sequencing to elucidate the underlying mechanisms triggering gene expression changes in wild-type aged mice. We found that in 2-year-old liver, 40% of elongating RNA polymerases are stalled, lowering productive transcription and skewing transcriptional output in a gene-length-dependent fashion. We demonstrate that this transcriptional stress is caused by endogenous DNA damage and explains the majority of gene expression changes in aging in most mainly postmitotic organs, specifically affecting aging hallmark pathways such as nutrient sensing, autophagy, proteostasis, energy metabolism, immune function and cellular stress resilience. Age-related transcriptional stress is evolutionary conserved from nematodes to humans. Thus, accumulation of stochastic endogenous DNA damage during aging deteriorates basal transcription, which establishes the age-related transcriptome and causes dysfunction of key aging hallmark pathways, disclosing how DNA damage functionally underlies major aspects of normal aging