FRIMEDBIO-Fri prosj.st. med.,helse,biol

We here aim both at exploring the causal links between growth rate, genome size and cell size and the evolutionary drivers for reduced genome size. There are likely several routes to genome size variability within and across taxa. Here, we are mainly inte rested in the observation that meiosis and cell division often is negatively correlated with genome size across plant and animal taxa. Since genome size and cell size also are tightly coupled, both cell and genome size should also show a strong negative c orrelation with developmental time. We hypothesize that this could be related to a phosphorus allocation from DNA to RNA under P-deficiency. A crucial question is thus the evolutionary drivers for reduced genome size in organisms, and how this actually i s solved by the organisms. We will study both the role of polyploidy and genome downsizing after polyploidization, and the role of non-coding elements (transposons, repetitive units) in the context of genome streamlining. Yet we will address the aspec t of genome streamlining on a broad scale, we will specifically study the material costs of producing nucleic acids, and how this may have relevance for the allocation of resources between DNA and RNA. A larger genome may result in higher investment into nucleic acids since the majority of the eukaryotic genomic DNA, including non-coding regions, may be transcribed. Our focus is on whether there are in fact energy and material costs that could select against large genomes. Such costs can be inferred from: (i) the existence of purely mechanical constraints related to faster and more efficient replication and metabolic activity in smaller genomes and cells; and (ii) the tight coupling of rapid growth and cellular rRNA copy numbers, meaning that high somatic N and P contents may represent a tradeoff between material resources allocated to DNA vs. RNA. The project will be based both on meta-analysis of existing data and by experiments with a range of organisms.