The insertion of transposable elements (TEs) can interrupt the coding sequences, alter gene expression and contribute to secondary rearrangements in genomes by acting as sites for additional mutational events such as duplications, deletions, inversions and translocations. Together, these often result in serious mutant phenotypes and have increasingly been shown to contribute to human diseases. To defend against the deleterious consequences of TEs, organisms have evolved complex surveillance and regulatory systems for TE detection and silencing. Mitigation of the deleterious consequences from insertional mutagenesis includes the ability to be excised from the mRNA of genes whose coding sequences are interrupted by a TE. An analysis of the C. elegans transposable element Tc1 into only three loci has suggested that the effects of Tc1 can be mitigated by splicing the Tc1 from the primary mRNA transcript4. Here I propose to test the generality of this observation in C. elegans strains that contain unusually large numbers Tc1 insertions using short-read RNA sequencing (Illumina). The DNA transposon Tc1 is regulated at approximately 30 copies in standard laboratory strains of C. elegans, Bristol N2. These Tc1 insertions usually reside in introns or intergenic regions. In contrast, the Bergerac strains of C. elegans contain 450- 750 copies of Tc1, of which many interrupt coding sequences of genes5. In addition to analyzing Tc1 splicing from mRNA, these strains additionally provide a unique opportunity to study the consequences of genic Tc1 insertions on (i) transcript abundance, both of the genes containing an insertion as well as neighboring genes and (ii) abundance of different mRNA isoforms transcribed from inserted genes, Lastly, I will test if splicing of Tc1 from primary transcripts differs between the germline and the somatic tissue.