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Kundu, A.

Publications and source records attributed to Kundu, A..

3 recordsLinked to original sources

Cross-Platform Mechanical Characterization of Lung Tissue

Published data on the mechanical strength and elasticity of lung tissue is widely variable, primarily due to differences in how testing was conducted across individual studies. This makes it extremely difficult to find a benchmark modulus of lung tissue when designing synthetic extracellular matrices (ECMs). To address this issue, we tested tissues from various areas of the lung using multiple characterization techniques, including micro-indentation, small amplitude oscillatory shear (SAOS), uniaxial tension, and cavitation rheology. We report the sample preparation required and data obtainable across these unique but complimentary methods to quantify the modulus of lung tissue. We highlight cavitation rheology as a new method, which can measure the modulus of intact tissue with precise spatial control, and reports a modulus on the length scale of typical tissue heterogeneities. Shear rheology, uniaxial, and indentation testing require heavy sample manipulation and destruction; however, cavitation rheology can be performed in situ across nearly all areas of the lung with minimal preparation. The Youngs modulus of bulk lung tissue using microindentation (1.9{+/-}0.5 kPa), SAOS (3.2{+/-}0.6 kPa), uniaxial testing (3.4{+/-}0.4 kPa), and cavitation rheology (6.1{+/-}1.6 kPa) were within the same order of magnitude, with higher values consistently reported from cavitation, likely due to our ability to keep the tissue intact. Although cavitation rheology does not capture the non-linear strains revealed by uniaxial testing and SAOS, it provides an opportunity to measure mechanical characteristics of lung tissue on a microscale level on intact tissues. Overall, our study demonstrates that each technique has independent benefits, and each technique revealed unique mechanical features of lung tissue that can contribute to a deeper understanding of lung tissue mechanics.

bioengineering

Transcriptomic analyses with the progress of symbiosis in ‘crack-entry’ legume Arachis hypogaea highlight its contrast with ‘Infection thread’ adapted legumes

In root-nodule symbiosis, rhizobial invasion and nodule organogenesis is host controlled. In most legumes, rhizobia enter through infection-threads and nodule primordium in the cortex is induced from a distance. But in dalbergoid legumes like Arachis hypogaea, rhizobia directly invade cortical cells through epidermal cracks to generate the primordia. Herein we report the transcriptional dynamics with the progress of symbiosis in A. hypogaea at 1dpi: invasion; 4dpi: nodule primordia; 8dpi: spread of infection in nodule-like structure; 12dpi: immature nodules containing rod-shaped rhizobia; and 21dpi: mature nodules with spherical symbiosomes. Expression of putative orthologue of symbiotic genes in crack-entry legume A. hypogaea was compared with infection thread adapted model legumes. The contrasting features were (i) higher expression of receptors like LYR3, EPR3 as compared to canonical NFRs (ii) late induction of transcription factors like NIN, NSP2 and constitutive high expression of ERF1, EIN2, bHLH476 and (iii) induction of divergent pathogenesis responsive PR-1 genes. Additionally, symbiotic orthologues of SymCRK, FLOT4, ROP6, RR9, NOOT and SEN1 were not detectable and microsynteny analysis indicated the absence of RPG and DNF2 homologues in diploid parental genomes of A. hypogaea. The implications are discussed and a molecular framework that guide crack-entry symbiosis in A. hypogaea is proposed.

plant biology

Small Molecules Attenuate the Interplay between Conformational Fluctuations, Early Oligomerization and Amyloidosis of Alpha Synuclein

Aggregation of alpha synuclein has strong implications in Parkinsons disease. The heterogeneity of folding/aggregation landscape and transient nature of the early intermediates result in difficulty in developing a successful therapeutic intervention. Here we used fluorescence measurements at ensemble and single molecule resolution to study how the late and early events of alpha synuclein aggregation modulate each other. The in-vitro aggregation data was complemented using measurements inside live neuroblastoma cells by employing a small molecule labeling technique. An inhibitor molecule (arginine), which delayed the late event of amyloidosis, was found to bind to the protein, shifting the early conformational fluctuations towards a compact state. In contrast, a facilitator of late aggregation (glutamate), was found to be excluded from the protein surface. The presence of glutamate was found to speed up the oligomer formation at the early stage. We found that the effects of the inhibitor and facilitator were additive and as a result they maintained a ratio at which they cancelled each others influence on different stages of alpha synuclein aggregation.

biophysics