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Biology subjects

Yeung, K. C.

Publications and source records attributed to Yeung, K. C..

2 recordsLinked to original sources

Cell-type specific autophagy in root hair forming cells is essential for salt stress tolerance in Arabidopsis thaliana

Autophagy is a vital cellular quality control pathway that enables plants to adapt to changing environments. By degrading damaged or unwanted components, autophagy maintains cellular homeostasis. While the organismal phenotypes of autophagy-deficient plants under stress are well-characterized, the contribution of cell-type-specific autophagy responses to whole-plant homeostasis remains poorly understood. Here, we show that root hair-forming cells (trichoblasts) of Arabidopsis thaliana exhibit higher autophagic flux than adjacent non-hair cells (atrichoblasts). This differential autophagy is genetically linked to cell fate determination during early development. Mutants disrupting trichoblast or atrichoblast identity lose the autophagy distinction between these cell types. Functional analyses reveal that elevated autophagy in trichoblasts is essential for sodium ion sequestration in vacuoles--a key mechanism for salt stress tolerance. Disrupting autophagy specifically in trichoblasts impairs sodium accumulation and reduces plant survival under salt stress. Conversely, cell-type-specific complementation restores both sodium sequestration and stress tolerance. Our findings uncover a cell-type-specific autophagy program in root hairs and demonstrate how developmental cues shape autophagy to enhance stress resilience. This work establishes a direct link between cell identity, autophagy, and environmental adaptation in plants.

plant biology↗

Critical role of miR-10b in BRafV600E dependent anchorage independent growth and invasion of melanoma cells

Recent high-throughput-sequencing of cancer genomes has identified oncogenic mutations in the BRaf genetic locus as one of the critical events in melanomagenesis. BRaf encodes a serine/threonine kinase that regulates the MAPK/ERK kinase (MEK) and extracellular signal-regulated kinase (ERK) protein kinase cascade. In normal cells, the activity of BRaf is tightly regulated and is required for cell growth and survival. BRaf gain-of-function mutations in melanoma frequently lead to unrestrained growth, enhanced cell invasion and increased viability of cancer cells. Although it is clear that the invasive phenotypes of BRaf mutated melanoma cells are stringently dependent on BRaf-MEK-ERK activation, the downstream effector targets that are required for oncogenic BRaf-mediated melanomagenesis are not well defined. miRNAs have regulatory functions towards the expression of genes that are important in carcinogenesis. We observed that miR-10b expression correlates with the presence of the oncogenic BRaf (BRafV600E) mutation in melanoma cells. While expression of miR-10b enhances anchorage-independent growth of BRaf wild-type melanoma cells, miR-10b silencing decreases BRafV600E cancer cell invasion in vitro. Importantly, the expression of miR-10b is required for BRafV600E-mediated anchorage-independent growth and invasion of melanoma cells in vitro. Taken together our results suggest that miR-10b is an important mediator of oncogenic BRafV600E activity in melanoma.

cancer biology↗