Cytoplasmic mRNA recapping is essential for stress recovery and intracellular proliferation in Trypanosoma cruzi

Trypanosoma cruzi , the causative agent of Chagas disease, regulates gene expression predominantly after transcription because it lacks conventional gene-specific promoters. Cytoplasmic mRNA recapping has been proposed to restore translation-competent mRNAs from silenced transcripts, but its physiological role in kinetoplastids has remained unclear. Here, we show that the cytoplasmic capping enzyme TcCe1 supports transcriptome homeostasis, an effective heat-shock response, and productive intracellular infection of host cells. TcCe1 loss was associated with reduced transcript abundance across extended polycistronic transcription units, impaired induction of proteostasis factors under stress, altered steady-state abundance of uncapped transcripts detected by ligation-mediated RT-qPCR, and marked defects in recovery and infectivity. Because cytoplasmic recapping in kinetoplastids is mechanistically distinct from host pathways, TcCe1 may represent a promising target for parasite-selective therapeutics. Together, our findings highlight the importance of TcCe1 in RNA-level regulation, environmental responsiveness, and host adaptation in this early-branching eukaryote.