Organisms employ sophisticated systems for genome defense against foreign and potentially harmful elements, while leaving room for gene adaptation. In animals, conserved PIWI Argonautes use genomically encoded small RNA guides (called piRNAs) to detect and silence foreign nucleotide sequences, such as transposons. In Caenorhabditis elegans, the detection of foreign transcripts by PIWI triggers the production of a second class of antisense small RNAs (called 22G-RNAs), which guide worm-specific Argonautes (WAGOs) to direct transcriptional and posttranscriptional silencing. PIWI-piRNA complexes recognize targets via imperfect base-pairing, which could threaten the expression of endogenous host genes. Nevertheless, worms use yet a third small RNA pathway involving the Argonaute CSR-1 to license endogenous germline gene expression and prevent inappropriate silencing by the PIWI pathway. How and why certain genes are licensed remains unknown. Here I show that introns and, by inference, mRNA splicing protect messenger RNAs from germline silencing. Intronless reporters encounter 22G-RNA-dependent and -independent silencing mechanisms, which we collectively termed “intronless silencing.” Genetic studies revealed that primary Argonautes, e.g., PIWI, are not required for the 22G-RNA-dependent intronless silencing mechanism, suggesting that intronless reporters are silenced by default. Nuclear and cytoplasmic WAGOs enabled the transmission of silencing from an intronless allele to a homologous intron-containing allele. The 22G-RNA-independent mechanism not only reduced intronless reporter mRNA levels, compared to the homologous intron-containing genes, but also prevented polyadenylation and nuclear export. Cis-acting elements that promote export from the nucleus nevertheless failed to fully activate expression of intronless reporters, suggesting additional layers of regulation in the small RNA-independent mechanism of intronless silencing. These findings suggest that multiple germline surveillance systems monitor transcript splicing, reveal a protective role of splicing in transcript licensing, and provide evidence for a splicing-dependent, sequence-independent mode of Argonaute programming.