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Manasa Bharathwaj

@mbharathwaj.bsky.social
54 followers 73 following 4 posts

Currently at New England Biolabs | Previously a Research Fellow in the Traven Lab, Monash Biomedicine Discovery Institute | Using this profile for the love of microbes 🦠🧫

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Manasa Bharathwaj @mbharathwaj.bsky.social · 21/08/2026
Hot off the press from the Traven lab! Check out for some fun videos on bacterial metabolites modulating fungal metabolism and morphogenesis in Candida albicans! Biggest thanks to Prof. Ana Traven and our collaborators at Warwick, Monash and Bio21. Thanks for sharing @evolvedbiofilm.bsky.social :)
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Manasa Bharathwaj @mbharathwaj.bsky.social · 24/03/2026
A very interesting take and article on the evolution of #AMR Looks like some bacteria just don't "cave in" to antibiotics. www.bbc.com/future/artic...
bbc.com
'Predators that just run in and grab, stab and kill': The deep cave bacteria resistant to modern medicine
In the brutal world of deep caves, bacteria live in a miniature world of terror. The weapons they have evolved can defeat antibiotics – but now they are inspiring powerful new drugs.
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Manasa Bharathwaj @mbharathwaj.bsky.social · 02/10/2025
Had a wonderful time at Brissy attending #ASBMB2025 at UQ while commuting by ferry! Thank you @asbmbaus.bsky.social Yeast SIG for the opportunity and support to present my work on fungi.
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Reposted by Manasa Bharathwaj
François Mayer @francoismayer.bsky.social · 29/07/2025
Evolution of antifungal resistance in the environment New Review Article by @normanvanrhijn.bsky.social and @drjorhodes.com Read it here: rdcu.be/eyobz www.nature.com/articles/s41...
rdcu.be
Evolution of antifungal resistance in the environment
Nature Microbiology - This Review discusses the evolution, emergence and expansion of environmental fungicide and antifungal drug resistance.
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Reposted by Manasa Bharathwaj
PLOS Biology @plosbiology.org · 23/05/2025
#Fungal infections are hard to treat due to #DrugResistance. @blakebillmyre.bsky.social &co use a high-throughput #TNseq system in #Cryptococcus neoformans to identify >1400 essential genes & reveal a role for #mitochondrial genes in #fluconazole sensitivity @plosbiology.org 🧪 plos.io/4dz3iVm
Schematic of TN-seq in C. neoformans. Top left: Transposon insertions (orange arrow) into nonessential genes results in viable cells. In contrast, insertions into essential genes will result in dead and nonrecoverable cells. Top right: TN-seq works by generating a library of cells where each cell has a single independent transposon insertion in a random location. As in A, those insertions into essential regions cause the cells to die and are nonrecoverable. As a result, the total library (bottom) is depleted in insertions in essential regions. Bottom: The Ac/Ds transposon was split into an Ac transposase and a Ds transposon containing a neomycin resistance marker. This Ds transposon was integrated into an intron of URA5 and the Ac transposase was integrated into the safe haven locus. The resulting stain is ura− and neomycin resistant. Upon initiating transposition via growth on galactose, the strain becomes URA+ and mutant at another locus (depicted here as YFG1).
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Reposted by Manasa Bharathwaj
The MRC Centre for Medical Mycology @mrccmm.bsky.social · 23/05/2025
Fascinating article about @normanvanrhijn.bsky.social work on the affects of climate change on fungi & fungal infections, with comments from MRC CMM's Elaine Bignell www.bloomberg.com/opinion/arti...
bloomberg.com
Deadly Fungi Are Here, and They’re Spreading
Unlike “The Last of Us,” virulent fungal disease isn't a work of science fiction.
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Reposted by Manasa Bharathwaj
Trevor Lithgow @trevor-lithgow.bsky.social · 20/05/2025
We are recruiting for a PhD student who wants to understand how bacterial membranes are built and how they function. It would be a biology meets maths project … if this piques your interest take a look here: macsys.org/monash-phd-s... for project details and contact info
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Reposted by Manasa Bharathwaj
Trevor Lithgow @trevor-lithgow.bsky.social · 01/05/2025
"That telomere phages are so prevalent means that they are a selective force, one that we know little about. We now want to understand how the telomere-toxin is secreted and also understand how this ‘telocin’ wheedles its way into unsuspecting bacterial neighbors” www.science.org/doi/10.1126/...
science.org
Telomere bacteriophages are widespread and equip their bacterial hosts with potent interbacterial weapons
Klebsiella host strains infected with telomere phages can grow to be the dominant lineage in mixed populations.
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