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Sulkshane, P.

Publications and source records attributed to Sulkshane, P..

3 recordsLinked to original sources

Phase separation as a concentrating mechanism of protein/peptide hormones for the secretory granule storage

Protein/peptide hormones in the regulated secretory pathway are stored within secretory granules (SGs) as densely packed aggregates for extended periods of time until their stimulated release. These aggregated dense cores are reported as functional amyloids for several pituitary hormones. However, the molecular events initiating hormone aggregation and SG biogenesis remain poorly understood. Using a diverse set of protein/peptide hormones with different sizes and structures, we demonstrated that all these hormones undergo phase separation in trans-Golgi network (TGN)-relevant conditions (including low pH, the presence of glycosaminoglycans, etc.), which rapidly transitioned into solid-like structures and eventually form amyloid fibrils. Further, the cellular model expressing two protein hormones (GH-EGFP and PRL-EGFP) showed the highly dynamic, liquid-like condensate formation at the TGN volume, which was transported via microtubule to the cellular periphery/tips and formed a ready pool of mature SGs containing amyloid-rich hormone aggregates. Importantly, both in vitro and cellular studies confirmed that solid-like amyloid aggregates are reversible and can release bioactive monomeric hormones, recapitulating regulated exocytosis. Together, our findings suggest hormone phase separation at the TGN as a common molecular principle for concentrating cargo, driving rapid functional aggregation, and ensuring efficient storage within SGs.

biochemistry↗

Hypoxia-induced mitoROS triggers M1 linear ubiquitin chains and activates NF-κB signaling

Mitochondria are essential organelles responsible for cellular energy production and metabolism. Hypoxia, a pathophysiological condition, impairs the electron transport chain, disrupts mitochondrial function, and produces harmful reactive oxygen species (ROS). Ubiquitin signaling regulates mitochondrial health through several mechanisms, including protein degradation and mitophagy. Here, we show that hypoxia-induced mitophagy occurs independently of ubiquitination. However, mitochondria are heavily ubiquitinated under hypoxic stress. A significant portion of these hypoxia-induced ubiquitin chains constitute a specific type: linear head-to-tail fusions (M1), which are known for their role in NF-{kappa}B activation during cytokine signaling. We demonstrate that hypoxia-induced mitochondrial ROS leads to the accumulation of these M1 chains, activating NF-{kappa}B signaling and increasing the expression of its target genes. These findings reveal a critical internal signal that helps cells adapt to mitochondrial stress and triggers an inflammatory response.

biochemistry↗

Signature activities of 20S proteasome include degradation of the ubiquitin-tag with the protein under hypoxia

Careful removal of unwanted proteins is necessary for cell survival. The primary constitutive intracellular protease is the 26S proteasome complex, often found in equilibrium with its free catalytic subcomplex- the 20S core particle. Protein degradation by 26S is tightly regulated by prior ubiquitination of substrates, whereas 20S is amenable to substrates with an unstructured segment. Differentiating their contributions to intracellular proteolysis is challenging due to their common catalytic sites. Here, by chemically synthesizing a synoptic set of homogenous ubiquitinated proteins, we ascribe signature features to 20S function and demonstrate a unique property: degrading the ubiquitin-tag along with the target protein. Cryo-EM confirms that a ubiquitinated substrate can induce asymmetric conformational changes to 20S. Mass-spectrometry of intracellular peptidome under hypoxia and in human failing heart identifies the signature properties of 20S in cells. Moreover, the ability of 20S proteasome to clear toxic proteins rapidly, contributes to better survival under these conditions.

biochemistry↗