Biology subjects

Hwang, S.-K.

Publications and source records attributed to Hwang, S.-K..

3 recordsLinked to original sources

bioRxiv2026

CRISPR/Cas12a-Mediated Knockout of the INNER NO OUTER (INO) Gene in Musa balbisiana cv. Bhimkol

Banana (Musa spp.) is a vital staple food and cash crop cultivated in over 140 countries, providing nourishment and livelihoods to more than 400 million people worldwide. In this context, Bhimkol (Musa balbisiana, BB genome), a diploid banana variety native to Northeast India holds significant nutritional and commercial value. Its high iron and nutrient content have already been commercially validated through products like Bhimvita and Bhimshakti, which utilize fresh fruit pulp as nutrient-rich food for infants. However, Bhimkol fruits typically contain 100-150 seeds, an undesirable trait for product development. The manual removal of these seeds significantly increases production time and labour costs. Furthermore, because bananas are recalcitrant to traditional breeding, there is a constant need for rapid in vitro transformation protocols. To address these challenges, as a proof of concept, our research aims to knockout the INNER NO OUTER (INO) gene, which is responsible for ovule development. Using CRISPR/Cas12a technology, we established an efficient and reproducible in vitro regeneration and transformation system using Embryogenic Cell Suspensions (ECS). The resulting CRISPR-edited plantlets exhibited various mutations, including insertions and deletions (INDELs) within the targeted INO gene. These INDELs resulted in frameshift mutations that triggered premature stop codons. While these genetic changes are expected to render the banana seedless, phenotypic verification is currently underway to confirm the absence of seeds in mature fruit. Significance StatementDespite its superior nutritional profile, the commercial viability of the Bhimkol banana (Musa balbisiana) is restricted due to abundance of seeds (100-150 per fruit). This study employs CRISPR/Cas12a-mediated knockout the INNER NO OUTER (INO) gene in Bhimkol and expected to develop seedless fruits. The resulting plantlets exhibit targeted indels that trigger frameshift mutations, effectively disrupting ovule developmental INO gene.

plant biology↗

bioRxiv2023

Restoring adiponectin via rosiglitazone ameliorates tissue wasting in mice with lung cancer.

The cancer associated cachexia syndrome (CACS) is a systemic metabolic disorder resulting in loss of body weight due to skeletal muscle and adipose tissues atrophy. CACS is particularly prominent in lung cancer patients, where it contributes to poor quality of life and excess mortality. Using the Kras/Lkb1 (KL) mouse model, we found that CACS is associated with white adipose tissue (WAT) dysfunction that directly affects skeletal muscle homeostasis. WAT transcriptomes showed evidence of reduced adipogenesis, and, in agreement, we found low levels of circulating adiponectin. To preserve adipogenesis and restore adiponectin levels, we treated mice with the PPAR-{gamma} agonist, rosiglitazone. Rosiglitazone treatment increased serum adiponectin levels, delayed weight loss, and preserved skeletal muscle and adipose tissue mass, as compared to vehicle-treated mice. The preservation of muscle mass with rosiglitazone was associated with increases in AMPK and AKT activity. Similarly, activation of the adiponectin receptors in muscle cells increased AMPK activity, anabolic signaling, and protein synthesis. Our data suggest that PPAR-{gamma} agonists may be a useful adjuvant therapy to preserve tissue mass in lung cancer. Key points- The PPAR-{gamma} agonist, rosiglitazone, restores circulating adiponectin levels in mice with lung cancer. - Rosiglitazone preserves skeletal muscle and adipose tissue mass in mice with lung cancer. - The preservation of muscle mass with rosiglitazone is associated with increases in AMPK and AKT activity. - Stimulation of adiponectin signaling increases AMPK activity, anabolic signaling, and protein synthesis in muscle cell culture.

cancer biology↗

bioRxiv2022

Epinephrine inhibits PI3K alpha via the Hippo kinases.

The phosphoinositide 3-kinase, p110, is an essential mediator of insulin signaling and glucose homeostasis. We systematically interrogated the human serine, threonine, and tyrosine kinome to search for novel regulators of p110 and found that the Hippo kinases phosphorylate and completely inhibit its activity. This inhibitory state corresponds to a conformational change of a membrane binding domain on p110, which impairs its ability to engage membranes. In human primary hepatocytes, cancer cell lines, and rodent tissues, activation of the Hippo kinases, MST1/2, using forskolin or epinephrine is associated with phosphorylation and inhibition of p110, impairment of downstream insulin signaling, and suppression of glycolysis and glycogen synthesis. These changes are abrogated when MST1/2 are genetically deleted or inhibited with small molecules. Our study reveals a novel inhibitory pathway of PI3K signaling and a previously unappreciated link between epinephrine and insulin signaling.

physiology↗