Biology subjects

Nama, S.

Publications and source records attributed to Nama, S..

3 recordsLinked to original sources

bioRxiv2026

Root-Suppressed Phenotype of Tomato Rs Mutant is Seemingly Related to Expression of Root-Meristem-Specific Sulfotransferases

Root development and growth are governed by a complex interplay between a plants genetic makeup and its ambient environment. In this study, we characterised a radiation-induced root-suppressed (Rs) mutant mapped on chromosome 4 of tomato. Rs seedlings had a dwarf stature, and mature plants exhibited abnormalities in their leaves, flowers, and fruits. The partial rescue of seedling root elongation by H2S donors or L-cysteine hinted that its root defect is linked to disrupted sulfur metabolism. The metabolite profiling of organs revealed altered homeostasis, analogous to that of plants subjected to sulfur starvation. Whole-genome sequencing revealed that the Rs genome was replete with genetic lesions; therefore, the pleiotropic morphological abnormalities likely emanate from mutations in other genes, including those related to sulfur. Among S-related genes, two sulfotransferase genes (Solyc04g028380 and Solyc04g028390) localised on chromosome 4 showed mutations in their promoters. The expression of both sulfotransferases is confined to the root meristem, suggesting a causal connection with the suppression of root growth. These sulfotransferases belonged to a distinct subset exclusively expressed in the root meristem and were distinct from the tyrosine sulfotransferase involved in the sulfation of root growth factors. Our study suggests that a sulfur-related module, other than tyrosine sulfotransferase, may regulate root development.

plant biology↗

bioRxiv2020

BRAWNIN: A sORF-encoded Peptide Essential for Vertebrate Mitochondrial Complex III Assembly

The emergence of small open reading frame (sORF)-encoded peptides (SEPs) is rapidly expanding the known proteome at the lower end of the size distribution1,2. Here, we show that the mitochondria proteome is enriched for proteins smaller than 100 a.a. (defined as SEPs). Using a mitochondrial prediction and validation pipeline for small open-reading-frame (sORF)-encoded peptides (SEPs), we report the discovery of 16 endogenous mitochondrial SEPs (mito-SEPs) associated with oxidative phosphorylation (OXPHOS). Through functional prediction, proteomics, metabolomics and metabolic flux modeling, we demonstrate that BRAWNIN (BR), a 71 amino acid peptide encoded by the C12orf73 gene, is essential for respiratory chain complex III (CIII) assembly. In human cells, BR is induced by the energy-sensing AMPK pathway, and its depletion impairs mitochondrial ATP production. In vivo, BR is enriched in muscle tissues and its maternal zygotic deletion in zebrafish causes complete CIII loss, resulting in severe growth retardation, lactic acidosis and early death. Our findings demonstrate that BR is essential for oxidative phosphorylation across vertebrate species. We propose that mito-SEPs are an untapped resource for essential regulators of oxidative metabolism.

cell biology↗

bioRxiv2019

Integrative analysis identifies key molecular signatures underlying neurodevelopmental deficits in Fragile X Syndrome

Fragile X syndrome (FXS) is an incurable neurodevelopmental disorder with no effective treatment. FXS is caused by epigenetic silencing of FMR1 and loss of FMRP expression. To investigate the consequences of FMRP deficiency in the context of human physiology, we established isogenic FMR1 knockout (FMR1KO) human embryonic stem cells (hESCs). Integrative analysis of the transcriptomic and proteomic profiles of hESC-derived FMRP-deficient neurons revealed several dysregulated pathways important for brain development including processes related to axon development, neurotransmission, and the cell cycle. We functionally validated alterations in a number of these pathways, showing abnormal neural rosette formation and increased neural progenitor cell proliferation in FMR1KO cells. We further demonstrated neurite outgrowth and branching deficits along with impaired electrophysiological network activity in FMRP-deficient neurons. Using isogenic FMR1KO hESC-derived neurons, we reveal key molecular signatures and neurodevelopmental abnormalities arising from loss of FMRP. We anticipate that the FMR1KO hESCs and the neuronal transcriptome and proteome datasets will provide a platform to delineate the pathophysiology of FXS in human neural cells.

neuroscience↗