Natalia Pardo Lorente
@NataliaPardoL
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Biomedical research.👩🏼🔬PhD student in @SdelciL. Passionate about cancer metabolism & epigenetics. “May love, not fear, be the engine of change."
Joined March 2020
We made it among the BEST PICTURES OF THE YEAR by @Nature
https://t.co/XgDgMrtgLu Beautiful image representing in red the nuclear localization of MTHFD2 in pluripotent colon organoids by @NataliaPardoL Find the manuscript here: https://t.co/cGb360CwmT
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Metabolic enzymes are taking on unexpected "second jobs" within the nucleus, where they orchestrate critical functions like cell division and DNA repair. The discovery by @SdelciL in @NatureComms can help develop new metabolism-based cancer therapies.
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In a second study, Dr. Marta García Cao and Dr. Lorena Espinar manipulate metabolic enzyme IMPDH2 and cause triple-negative breast cancer cells to self-destruct, showcasing the value of targeting the 'moonlighting' enzymes in the nucleus.
nature.com
Nature Communications - Metabolism plays an important role in response to DNA damage, however the underlying mechanisms are less clear. Here, the authors identify a non-canonical role of IMPDH2...
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In the first study, the group show that the nucleus relies on MTHFD2 to maintain the integrity and stability of the genome. "The nucleus isn't just a passive storage space for DNA; it has its own metabolic needs and processes," says @NataliaPardoL.
nature.com
Nature Communications - The nuclear localization of metabolic enzymes is fascinating and in most cases remains a mystery. Here, Pardo Lorente and colleagues show that nuclear MTHFD2 is required for...
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Today we are publishing 2 MANUSCRIPTS in @NatureComms 1. @NataliaPardoL discovers the role of nuclear MTHFD2 in centromere stability 2. Espinar and Garcia-Cao reveal the role of nuclear IMPDH2 in the DNA damage response. Nuclear Metabolism is on 🔥
Metabolic enzymes are taking on unexpected "second jobs" within the nucleus, where they orchestrate critical functions like cell division and DNA repair. The discovery by @SdelciL in @NatureComms can help develop new metabolism-based cancer therapies.
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📣 Just published: @NataliaPardoL and @SdelciL 's review on MTHFD2 in healthy and cancer cells in npj Metabolic Health and Disease: https://t.co/Qh63dZ4qtV
#npjmetabhealth
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The review I wrote at the end of my PhD about the diverse roles of the fascinating enzyme MTHFD2 in health and disease is out! 🤩
If you want to know everything about #MTHFD2's canonical and non-canonical functions, check out @NataliaPardoL's just-published review. @Nature_NPJ
@ERC_Research @Boehringer Ingelheim Fonds PhD fellowship @CRGenomica 👇👇👇👇 https://t.co/F8FaQdMSUL
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Congratulations @RitobrataGhose and @fabio_pezzano for such nice and exciting NAM story! 👏🏼🤩🔥
The @SdelciL is on 🔥 --> WE PROMISE THIS IS THE LAST PREPRINT OF THE YEAR! THE 🍒 ON THE 🍰 Mitochondrial-nuclear energy crosstalk to defeat confinement stress. by @RitobrataGhose and @Fabio_Pezzano (@Ruprecht_lab)!
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Very proud of this collaborative effort of the Sdelci lab 💪🏼 Metabolic enzymes sitting on chromatin are very cool! 🤩
ARE METABOLIC ENZYMES ON CHROMATIN? Yes, they are ⤵️! We optimized a chromatin enrichment protocol to improve the extraction of chromatin-bound proteins (chromatome) and applied it to > 140 samples, including cancer cell lines and healthy epithelia from 10 different tissues. 🧵
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We are very happy to share with you the last paper of the Sdelci Lab published in @EmboMolMed where we decipher a new molecular mechanism for triple-negative breast cancer proliferation https://t.co/frJ2cIxjqI. Follow us in this threat!🧵
link.springer.com
EMBO Molecular Medicine - Triple‐negative breast cancer (TNBC) often develops resistance to single‐agent treatment, which can be circumvented using targeted combinatorial approaches....
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🥇 PhD of the lab👏👏👏👏 We present you RADIANT Dr. @NataliaPardoL from the Sdelci lab! Fantastic thesis and defense 🎉🎉 Thanks to the tribunal @MariaRodrColman @MarcusBuschbeck @ludicroce for their fantastic work! @CRGenomica #ProudMoment MTHFD2 #Cancer #metabolism
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I would also like to thank @Boehringer for awarding me a BIF PhD fellowship, and @ERC_Research @CienciaGOB and @CRGenomica for supporting our research!
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I would like to thank the whole team for the great effort that led to such a beautiful story 👏🏼👏🏼
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These results raise very interesting questions! Is this novel function of MTHFD2 in mitosis cancer-specific? Or is it conserved in physiological conditions, such as in embryogenesis? 👶🏻
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MTHFD2 is such an interesting enzyme! Our discovery reveals a nuclear moonlighting role for the cancer target MTHFD2, emphasizing that the unconventional localization of metabolic activities can impact the fate of mitosis. 💡
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In conclusion, nuclear MTHFD2 ensures an adequate centromeric methylation and expression so that mitosis can be completed correctly! 🤩
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Interestingly, the supplementation with the methyl donor SAM or folate metabolites does not recover the methylation defect, suggesting that the precise nuclear localization of MTHFD2 is required to maintain a unique metabolic environment needed for centromere methylation!📍
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Besides, treating cancer cells with a nuclear-specific MTHFD2 inhibitor recapitulated the mitotic and methylation defects observed upon MTHFD2 loss! 💊
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But how can we be sure that this novel role in mitosis is coming from the nuclear pool and not mitochondrial MTHFD2? Interestingly, CRISPR-engineered cells with MTHFD2 ONLY in the nucleus have a normal methylation and mitotic phenotype, with no mitotic defects. ✅
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We reasoned that this would alter centromere stability and hence lead to problems in mitosis…🧫 Indeed, upon MTHFD2 loss, cancer cells showed a reduced mitotic index and chromosome congression and segregation defects, which resulted in chromosomal structural alterations.🔬
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