Rpl3l, ribosomal protein L3-like, is a paralog of RPL3. It is specifically expressed in heart and skeletal muscle. Rpl3l-containing ribosomes play a role in determining translation elongation dynamics, which is crucial for cardiac function [1]. It is also involved in pathways related to cardiac muscle contraction and dilated cardiomyopathy [1]. Mouse models are valuable for studying Rpl3l's function.

In Rpl3l knockout male mice, there is impaired cardiac contractility, and ribosome occupancy at mRNA codons is altered in the heart, with changes negatively correlated to those in myoblasts overexpressing RPL3L. Rpl3L-containing ribosomes are less prone to collisions compared to canonical RPL3-containing ribosomes. The loss of Rpl3l-containing ribosomes affects translation elongation dynamics across the transcriptome, especially for transcripts related to cardiac muscle contraction and dilated cardiomyopathy, reducing the abundance of encoded proteins [1].

Rpl3l gene-deleted mice show no overt changes in cardiac structure or function at baseline or after pressure overload hypertrophy, likely due to up-regulation of RPL3. However, by 18 months, Rpl3l -/- null mice have significantly smaller hearts [2]. Deletion of Rpl3l triggers a compensation mechanism where RPL3 is up-regulated, and depletion of RPL3L leads to increased ribosome-mitochondria interactions and higher ATP levels in cardiomyocytes [3].

In conclusion, Rpl3l is essential for cardiac function through its role in translation elongation dynamics. Studies using Rpl3l knockout mouse models have revealed its significance in cardiac muscle contraction-related processes and dilated cardiomyopathy. These models have provided insights into the gene's function and the potential molecular mechanisms underlying heart-related diseases.