Next-generation sequencing has turned functional genomics into a high-throughput discipline, making it routine to score the fitness impact of tens of thousands of perturbations in a single experiment. Standard CRISPRi workflows, however, still rely on DNA-targeting dCas9 or dCas12. These effectors must find a protospacer-adjacent motif (PAM), thread through local chromatin, and tolerate host base modifications, constraints that leave blind spots in coverage. The limitations are even sharper for RNA viruses and phage genomes packed with non-canonical bases, where many loci remain inaccessible and functional maps fall short of full resolution. Conventional CRISPR-based screens focus on DNA and therefore run into well-known obstacles: strict PAM requirements, chemically modified bases, and the protein shells that some jumbo phages assemble around their chromosomes. To circumvent these barriers, I redirected the intervention point to RNA. The resulting platform, CRISPRi-ART, employs a nuclease-inactive Cas13d from Ruminococcus flavefaciens (dRfxCas13d) as a programmable RNA-binding repressor. Because Cas13d engages single-stranded messenger RNA directly, it operates independently of PAM motifs and is unaffected by DNA modifications that block Cas9 or Cas12. Systematic tiling in Escherichia coli uncovered a consistent vulnerability: when dCas13d binds within roughly seventy nucleotides of the ribosome-binding site, translation efficiency drops by as much as three orders of magnitude. This empirical window enabled a streamlined design of seven guides per gene, providing genome-wide coverage in a single library while maintaining strong, reproducible knock-down. CRISPRi-ART was first put to the test against a long-standing obstacle in phage biology: functional annotation of viruses that evade DNA-focused tools because their genomes are heavily modified or sequestered inside protein shells. Using the platform on a panel of coliphages with single-stranded RNA, single-stranded DNA, and double-stranded DNA genomes, I pinpointed viral genes that are indispensable for infection. Guides directed to the ribosome-binding sites of core structural and replication genes halted infection across this diverse set. A focused survey of the conserved rIIA-rIIB locus in T-even-related phages showed that these genes routinely disable host RexAB immunity, even when sequence identity is low. Transcriptome-wide libraries extended the analysis, generating fitness landscapes that flagged 2 more than ninety previously unannotated genes required for productive growth. The method also succeeded against nucleus-forming jumbo phages, demonstrating that RNA-level targeting can circumvent viral compartments that exclude DNA nucleases and silence transcripts needed for virion assembly. I next turned the method on the host itself, running genome-scale CRISPRi-ART screens across the complete E. coli transcriptome. A compact, seven-guide library built from the RBS susceptibility rules was assayed under varied nutrient and stress regimes. The screens recovered roughly half of the established essential proteome and exposed context-dependent weak spots that appear only during shifts in carbon source or oxidative stress. Because CRISPRi-ART blocks translation rather than transcription, downstream genes in polycistronic operons remain expressed, sidestepping the polar effects that complicate DNA-based CRISPR interference in polycistronic organisms. Guide alone control experiments without the effector, showed effect sizes that could not be differentiated from background, emphasizing the need for the RNP complex for effective knockdown at the ribosome-binding site. CRISPRi-ART also opened a window on post-transcriptional control. By tiling guides across small RNAs, antisense transcripts, and riboswitch leaders, the screen pinpointed nucleotide stretches whose silencing shifts downstream gene output. These maps, collected under changing temperature, carbon source, and oxidative stress, give a functional readout that complements traditional RNA-seq and structure probing, adding a practical route to annotate regulatory RNAs at scale. In sum, CRISPRi-ART clears the most persistent bottlenecks in genome-wide functional analysis. By working at the RNA level, it sidesteps PAM constraints, DNA base modifications, and physical barriers that limit traditional CRISPR methods, making the platform broadly useful across bacterial, phage, and non-coding landscapes. Its straightforward guide design and high ontarget specificity enable systematic studies that reach from operon architecture to host-virus cross-talk and RNA regulation. These strengths position CRISPRi-ART as a practical engine for strain optimization, designer phage discovery, and plug-and-play control of synthetic networks. Looking ahead, multiplex guide sets and combinatorial knock-downs should push the method further, turning transcriptome-scale screens into a routine tool for mapping and engineering complex genetic systems.