Recent Publications Harnessing the Power of Translatomics

Every week we provide a digest of a small number of recent interesting papers in the field of translatomics.

In this week’s Sunday papers,

  • Han et al. investigate the role of translation machinery in the biogenesis of phased, secondary, phasiRNAs during maize anther development.
  • Liu et al. use ribosome profiling and single-cell RNA-Seq to examine the molecular mechanisms behind pigeon lactation.
  • Surya et al. detail the impacts of ribosomal protein haploinsufficiency on mitochondrial function.

Ribosome binding of phasiRNA precursors accelerates the 24-nt phasiRNA burst in meiotic maize anthers

The Plant Cell, 2025.

Han, Y., Jiang, S., Dong, X., Dai, X., Wang, S., Zheng, Y., Yan, G., Li, S., Wu, L., Walbot, V., Meyers, B.C., and Zhang, M.

Sunday Paper 1

Phased, secondary, small interfering RNAs (phasiRNAs) are a specialized class of small RNAs essential for the development of anthers in grasses like maize and rice. PHAS precursor RNAs are often found attached to ribosomes on the endoplasmic reticulum in maize, however the mechanisms by which ribosome binding influences phasiRNA biogenesis are not yet fully understood. In this article, the authors investigate the role of translation machinery in the biogenesis of phased, secondary, phasiRNAs during maize anther development. They used ribosome profiling (Ribo-seq) in conjunction with RNA-seq across 10 developmental stages of maize anthers to explore why 24-nt phasiRNA precursors, previously thought to be non-coding, are enriched on ribosomes. Ribo-seq data revealed that ribosomes specifically bind to 24-PHAS transcripts, with binding levels peaking during the initiation of meiosis. This pattern closely mirrors the timing and abundance of 24-nt phasiRNA production. Ribosomes were found to be predominantly enriched in the 5′ regions of the precursors, specifically upstream of the miR2275 target sites. This conservation across different maize inbred lines suggests a functional evolutionary role.

The study also identified short open reading frames (sORFs) within these ribosome-binding regions. While Ribo-seq showed a characteristic 3-nt periodicity (indicating active ribosome movement), mass spectrometry failed to detect any stable translated peptides, suggesting the act of binding is more critical than the protein product. By using CRISPR/Cas9 to delete ribosome-binding regions, the authors demonstrated that losing ribosome occupancy significantly decreased 24-nt phasiRNA production without affecting the steady-state levels of the precursor transcripts themselves. They conclude that ribosomes act as a physical platform or recruitment hub on 24-PHAS transcripts, facilitating the biochemical transition from precursor RNA to small RNA, thereby “accelerating” the phasiRNA burst essential for male fertility in plants.

Learn more about EIRNABio’s ribosome profiling services here.

Ribosome profiling and single-cell RNA sequencing identify the unfolded protein response as a key regulator of pigeon lactation

Zoological Research, 2025.

Liu, J., Liu, S.F., Mao, H.R., Jiang, H.X., Liu, S.B., Xu, X.F., Wu, J.T., Liu, X., Zhang, W.T., Hu, X.L. and Chen, B.

Sunday Paper 2

Here, the authors investigate the molecular mechanisms behind pigeon lactation, a unique physiological process where both parents produce “crop milk” to nourish their young. Unlike mammalian milk, pigeon crop milk is a holocrine secretion composed of protein- and lipid-rich epithelial cells shed from the crop lining. Pigeon lactation involves a dramatic transformation of the crop tissue, characterized by rapid cell proliferation and a massive surge in protein production. While hormones like prolactin were known to trigger this, the precise cellular transitions and the regulatory “quality control” mechanisms required to handle such a high protein load remained poorly understood. The study combined three high-resolution technologies to map this transformation.

scRNA-seq (Single-Cell RNA Sequencing) identified the cellular “atlas” of the crop, revealing that basal and intermediate epithelial cells are the primary drivers of lactation. It mapped the trajectory of these cells as they differentiate into “lactating” cells, characterized by high metabolic activity. RNA-seq captured the global shifts in gene expression, confirming a massive upregulation of genes related to protein synthesis, lipid metabolism, and cell cycle progression during the lactating phase. Crucially, ribosome profiling (Ribo-seq) revealed that many genes involved in the Unfolded Protein Response (UPR) were being translated at much higher rates than their mRNA levels suggested. This proved that the crop manages the “stress” of massive protein synthesis through active translational regulation. The study concludes that the UPR pathway (specifically the Xbp1s branch) acts as a master regulator. It ensures the endoplasmic reticulum can handle the enormous protein folding demand, preventing cell death during the peak of lactation. This research provides a definitive molecular model for how non-mammals achieve high-output “lactation” through specialized cellular stress management

Learn more about EIRNABio’s ribosome profiling services here.

Differential impacts of ribosomal protein haploinsufficiency on mitochondrial function

Journal of Cell Biology, 2025.

Surya, A., Bolton, B.M., Rothe, R., Mejia-Trujillo, R., Leonita, A., Zhao, Q., Arya, A., Liu, Y., Rangan, R., Gorusu, Y., Nguyen, P., Cenik, C., and Sarinay Cenik, E.

Sunday Paper 3

In this article, the authors examine the molecular consequences of ribosomal protein (RP) haploinsufficiency, a condition linked to “ribosomopathies” like Diamond-Blackfan anemia. While it is known that reducing RP levels affects global translation, this study explores why different RP deficiencies lead to distinct clinical and cellular phenotypes, specifically focusing on mitochondrial dysfunction. Ribosomal proteins are essential for assembling the machinery that builds all cellular proteins. When one copy of an RP gene is lost (haploinsufficiency), it doesn’t just slow down protein synthesis across the board; it often leads to highly specific defects. The researchers sought to understand how these deficiencies selectively impair mitochondria, which rely on a delicate balance of proteins encoded by both the nucleus and the mitochondrial genome.

RNA-seq revealed that while many mitochondrial genes were transcribed normally, ribosome profiling (Ribo-seq) showed a significant drop in their translation. This indicates that mitochondrial failure in these cells is primarily a translational regulation issue. Ribo-seq data identified that specific mRNAs, particularly those encoding components of the Electron Transport Chain (ETC), are hyper-sensitive to reduced ribosome levels. By comparing different RP mutants, the researchers found that not all RPs are equal; some deficiencies specifically trigger the Integrated Stress Response (ISR), further dampening the translation of mitochondrial proteins and leading to a collapse in oxidative phosphorylation. The study concludes that RP haploinsufficiency creates a “translational bottleneck” that disproportionately hits mitochondrial genes. This creates a feedback loop of cellular stress, providing a mechanistic explanation for how basic ribosome defects manifest as complex metabolic and mitochondrial diseases.

Learn more about EIRNABio’s ribosome profiling services here.