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Manasa Bharathwaj

@mbharathwaj.bsky.social

Research Fellow | Traven Lab | Monash Biomedicine Discovery Institute | Molecular biologist using bacterial metabolites to study fungi ๐Ÿฆ ๐Ÿงซ | Meme enthusiast

38 Followers  |  66 Following  |  1 Posts  |  Joined: 25.03.2025  |  1.4497

Latest posts by mbharathwaj.bsky.social on Bluesky

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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.

02.10.2025 01:03 โ€” ๐Ÿ‘ 2    ๐Ÿ” 0    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0
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Evolution of antifungal resistance in the environment Nature Microbiology - This Review discusses the evolution, emergence and expansion of environmental fungicide and antifungal drug resistance.

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...

29.07.2025 17:56 โ€” ๐Ÿ‘ 6    ๐Ÿ” 3    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 1
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 uraโˆ’ and neomycin resistant. Upon initiating transposition via growth on galactose, the strain becomes URA+ and mutant at another locus (depicted here as YFG1).

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 uraโˆ’ and neomycin resistant. Upon initiating transposition via growth on galactose, the strain becomes URA+ and mutant at another locus (depicted here as YFG1).

#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 ๐Ÿงช plos.io/4dz3iVm

23.05.2025 10:15 โ€” ๐Ÿ‘ 19    ๐Ÿ” 10    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 0
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Deadly Fungi Are Here, and Theyโ€™re Spreading Unlike โ€œThe Last of Us,โ€ virulent fungal disease isn't a work of science fiction.

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...

23.05.2025 09:13 โ€” ๐Ÿ‘ 6    ๐Ÿ” 4    ๐Ÿ’ฌ 0    ๐Ÿ“Œ 0
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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 โ€ฆ if this piques your interest take a look here: macsys.org/monash-phd-s... for project details and contact info

20.05.2025 10:56 โ€” ๐Ÿ‘ 14    ๐Ÿ” 14    ๐Ÿ’ฌ 1    ๐Ÿ“Œ 1
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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.

"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 โ€˜telocinโ€™ wheedles its way into unsuspecting bacterial neighborsโ€

www.science.org/doi/10.1126/...

01.05.2025 22:04 โ€” ๐Ÿ‘ 107    ๐Ÿ” 61    ๐Ÿ’ฌ 7    ๐Ÿ“Œ 6

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