Dmitry Knorre

[Dmitry Knorre @dmkno]

3/3 I am especially happy that during this study, we gained valuable experience in the batch analysis of flow cytometry data using multimode, flowCore, and related R libraries.

[Dmitry Knorre @dmkno]

1/3 Another article we’ve published by the end of this year: https://t.co/oVwkYoJwpW. We took advantage of the fact that in yeast, mtDNA contributes to about 20% of total DNA amount. Therefore, it can be semi-quantitatively assessed using flow-cytometry at the single-cell level.

[Dmitry Knorre @dmkno]

2/3 Yeast strains with large deletions in mtDNA appeared to be highly heterogeneous in mtDNA amount. This suggests that the regulation of yeast cells' mtDNA copy number is disrupted by mutations in mtDNAs. As a result, mtDNA/nDNA ratio drifts with generations.

[Dmitry Knorre @dmkno]

3/3 This study began as a summer practice on molecular biology with a group of FBB students in the White Sea in 2021. I am glad that they (and we) persevered with the study, ended in this publication, despite our strenuous times.

[Dmitry Knorre @dmkno]

1/3. In this study, we found several unusual features in the mitochondrial genome of marine polychaete worm, Polydora ciliata (https://t.co/hVtUgLeuev).

[Dmitry Knorre @dmkno]

2/3 These regions (ORFans) are transcribed; furthermore, comparative genomic analysis suggests they encode proteins (dn/ds < 1). We suggest that these ORFans emerged as a result of the duplication of standard mitochondrial genes, followed by rapid evolution.

[Dmitry Knorre @dmkno]

Just out. Yeast can detect xenobiotics and induce drug-efflux systems, to get rid of them. High concentrations of tyrosol, yeast own secondary metabolite, also induce drug-efflux. #Yeast #DrugResistance #Metabolism 🧪🔬🧬

[Frontiers - Microbiology @FrontMicrobiol]

New Research: Tyrosol induces multiple drug resistance in yeast Saccharomyces cerevisiae #microbiology https://t.co/pcFKC3uGmZ

[Dmitry Knorre @dmkno]

@LidskyPeter Moorad an Co: "The strength of age-specific selection is maximized and constant throughout the prereproductive ages but must decline
over time until converging with zero at the last age of reproduction [11]."

[Dmitry Knorre @dmkno]

@LidskyPeter Moorad and Co argues against the predicted effects of extrinsic mortality but not about the theory in general. I did not know their reasonings, but it is not crucial for the concept. Anyway, they did not argue against selection shadows and doi: 10.1016/0022-5193(66)90184-6.

[Dmitry Knorre @dmkno]

@LidskyPeter I need to read the text of the math article, but I know the guppi paper. You can see that the authors consider their finding as an contradiction to a generaly accepted theory (see references within that paper!) and suggest some explanation why did they found opposit trend.

[Dmitry Knorre @dmkno]

@LidskyPeter Because flight and high body weight decreases age-independent hazard and, therefore, push back the selection shadow. Furthermore, selection shadow aggravates with the number of produced progeny. Birds and elephants longevity nicely fit the theory.

[Dmitry Knorre @dmkno]

@LidskyPeter Penna model is just a very simple implementation (illustration) of Medawar's theory. There is nothing more in it. But IMHO it is invincivle in its simplicity. I suggest, you underestimates de novo mutations in germline, most of which are slighlty deleterious

[Dmitry Knorre @dmkno]

@LidskyPeter See for example: DOI 10.1016/j.cub.2008.04.070
Moreover, Williams antagonistic pleiotropy is just an addition to the mutation accumulation theory. Do you reject it as well?

[Dmitry Knorre @dmkno]

@LidskyPeter The model illustrate that even population of the immortal organisms eventually accumulates 'deleterious in late life' alleles if there are possibility of such alleles in principle. There are some (although not so many) emperical and experimental confirmations of the theory.

[Dmitry Knorre @dmkno]

@LidskyPeter Mathematically yes. But in populations with small Ne deleterious mutations can be fixed becuase of stochastic reasons. Did you ever try running bit string Penna model of aging? It is very helpful to catch mutation accumulation theory concept (I did, it's fun).

[Dmitry Knorre @dmkno]

@LidskyPeter Adaptive or effectively neutral. Each genetically encoded system in an organism is under the mutational meltdown pressure and eventually degrade without selection. Therefore, I don't see a way how mutation accumulation theory can be wrong.

[Dmitry Knorre @dmkno]

@LidskyPeter Why wrong? Aging in the wild does not contradict to Medawar's mutation accumulation theory. Selection shadow gradually increases, therefore the theory predicts mortality rate starts to increase after puberty (and thus consistent with aging in the wild)

[Dmitry Knorre @dmkno]

Marine polychaete Polydora mitogenomes contain regions that likely to encode proteins missing in all other invertebrates. This taxon might provide a unique opportunity to explore gene neofunctionalization in mtDNA.

[bioRxiv Evobio @biorxiv_evobio]

ORFanes in mitochondrial genomes of marine polychaete Polydora https://t.co/twxf8oWCN4 #biorxiv_evobio

[Dmitry Knorre @dmkno]

3. Our findings suggest that yeast communities can benefit if a fraction of the cells randomly reduces polyene resistance.

[Dmitry Knorre @dmkno]

1. The role of regulated cell death in unicellular organisms is a matter of debate. In this article, we showed that dead yeast cells can save living cells by absorbing polyene antifungals.
https://t.co/Nm9RK4cGq4
#yeast #celldeath #antifungals

[Dmitry Knorre @dmkno]

2. The most striking result: by adding polyene-hypersensitive yeast cells we can save wild-type yeast cells from polyene macrolides. Adding just more wild-type cells doesn't work.
https://t.co/mSu0mXt3wt