Project description:As an adaptive response to the environment, oaks have evolved long taproots that increase their ability to acquire water. Taproots penetrate deeper layers of soil and send out absorptive roots that can then uptake water from these layers. This ability enables taproots to supply trees with water better. Unfortunately, the applied agrotechnical procedures during seedlings production in container nurseries damage the oaks' taproot, leading to changes in the root system structure. That changes may make the seedlings more responsive to chronic or periodic episodes of severe drought. In turn, seedlings that containers do not restrict roots growth, i.e. grown in rhizotron, may elongate because they are not subjected to air-pruning. Despite their significant role, little is known about the internal factors (specific genes) and their interactions that regulate taproot elongation in oaks seedlings. Thus, our study aimed to determine the potential genes regulating growth, cessation and physiology of taproot and check whether there is a difference in the expression level of the genes involved in root development. For this purpose, we performed next-generation sequencing (NGS), taproots and lateral roots, which allowed us to obtain a complete picture of the transcriptomes. Our findings of taproot growth regulations can be used to improve trees production in forest nurseries.
Project description:Multiple individuals sampled from across all 7 species of the American live oaks, and outgroup samples from the white oaks, red oaks, and golden oaks. Raw sequence reads
Project description:we performed Native Elongating Transcript Sequencing (NET-seq) on an rpa12Δ strain of S. cerevisiae and evaluated the resultant change in Pol I occupancy throughout the 35S gene and the IGS. Compared to WT, we observed template sequence-specific changes in Pol I occupancy throughout the 35S gene. We also observed rpa12Δ Pol I occupancy downstream of both termination sites and throughout most of the IGS, including the 5S gene. Occupancy of rpa12Δ Pol I increased just upstream of the promoter proximal Reb1 binding site and dropped significantly after, implicating this site as a third terminator for Pol I transcription.
