Biology subjects

Prasad, T.

Publications and source records attributed to Prasad, T..

3 recordsLinked to original sources

bioRxiv2025

Multimodal lesion mapping in affective blindsight reveals dual amygdala and superior temporal sulcus contributions to nonconscious emotion processing

Affective blindsight, the capacity to discriminate emotional stimuli despite bilateral damage to the primary visual cortex (V1) and without conscious awareness, offers a unique model of non-conscious visual processing. Subcortical pathways involving the pulvinar and amygdala have been proposed, but putative cortical contributions remain unclear. We examined 182 patients, including 31 with bilateral V1 lesions. Among these, 15 had cortical visual loss and 7 showed affective blindsight. Using behavioral testing, lesion symptom mapping, and tractography, we found that preserved pulvinar connectivity with both the posterior superior temporal sulcus (STS) and the amygdala is necessary for affective blindsight. These findings provide causal evidence for a multi-route architecture, identifying the pulvinar-STS pathway, alongside the pulvinar-amygdala pathway, as a critical substrate for non-conscious affective processing.

neuroscience↗

bioRxiv2024

DIS3L2 is essential for neural crest survival by modulating Akt signaling

DIS3 like 3-5 exoribonuclease 2 (DIS3L2), an exoribonuclease is known to preferentially degrade uridylated RNA substrates, miRNAs, and ncRNAs. Recent reports show that DIS3L2 also plays a key role in cell proliferation and tumor growth. Mutations in DIS3L2 are associated with congenital disorders such as Perlman syndrome, yet the developmental functions of DIS3L2 remain unknown. We report the developmental role of dis3l2 in neural crest specification, patterning, and survival in the zebrafish embryo. Dis3l2 morphants exhibited reduced expression of neural crest specifier genes coupled with extensive apoptosis in the neural tissue. Our study demonstrates that DIS3L2 regulates neuronal apoptosis and progenitor functions through the Akt -GSK3{beta} signaling pathway. Additionally, we show that DIS3L2 is essential for early mitoses in the zebrafish blastula and plays a key role in maintaining spindle length at metaphase, chromosome congression, spindle pole integrity, and cytokinesis. In summary, we identify new functions of exoribonuclease DIS3L2 in cell fate specification, neural progenitor survival, and mitosis during embryogenesis which form the underlying basis of DIS3L2-associated overgrowth Perlman syndrome. Plain English summaryDIS3 like 3-5 exoribonuclease 2 (DIS3L2) degrades mRNAs and various RNA substrates in the eukaryotic cells. DIS3L2 mutations are associated with congenital overgrowth syndromes like Perlman syndrome and Wilms tumor. The role of DIS3L2 in regulating the embryonic processes remains poorly understood. Our study delineates the developmental functions of DIS3L2 in cell fate determination, survival, and proliferation during vertebrate embryogenesis using zebrafish embryos as a model. We show that DIS3L2 plays a key role in neural crest survival and patterning by modulating Akt-GSK{beta} signaling. We also report unique molecular functions of DIS3L2 in mitotic fidelity and cytokinesis during embryonic mitoses. Our study provides novel insights into the molecular functions of DIS3L2 in regulating neuronal apoptosis during embryonic brain morphogenesis and associated CNS disorders.

developmental biology↗

bioRxiv2024

Developmental functions of rapgef1b in neural crest specification and presomitic mesoderm patterning

RAPGEF1, a guanine nucleotide exchange factor, regulates signaling and cytoskeletal dynamics in mammalian cells, yet its role in development remains unclear as Rapgef1 null mouse embryos do not survive beyond implantation. We demonstrate that zebrafish rapgef1 is maternally expressed, and its paralogs, rapgef1a and rapgef1b, exhibit tissue and developmental stage-specific splicing. Disruption of rapgef1b caused brain and somite defects, impaired cranial neural crest specification, and microcephaly-like phenotypes, uncovering its previously uncharacterized functions in morphogenesis and tissue patterning. Transcriptomic analyses and differential gene expression provide fresh insights into the developmental functions of rapgef1b in presomitic mesoderm and somitogenesis by modulating the Wnt/{beta} catenin signaling. Rapgef1b deficient embryos also showed spindle pole disorganization and chromosome mis-congression, linking Rapgef1 to centrosome-mediated mitotic fidelity. Together, our findings identify Rapgef1b as a key regulator of neural crest development, mesodermal morphogenesis, and early mitoses, highlighting its tissue-specific functions during vertebrate embryogenesis. TeaserIn this study, we show that rapgef1b is essential for shaping the embryonic brain, somites, and body axis by regulating gene expression, cell division, survival, and differentiation. Our findings reveal a new dimension of signaling-mediated cell fate specification during early vertebrate development.

developmental biology↗