Ana Martínez Gómez

Bibliography:

1. Monaghan and Haussmann 2006, Trends Eco & Evo 21, no. 1: 47–53.
2. Kappei and Londoño‐Vallejo 2008, Mech Ageing Dev, doi.org/10.1016/j.ma....
3. Olsson et al. 2018, Phil Trans R Soc B, doi.org/10.1098/rstb....

🧩 Take-home message: Hatchling telomere length in sand lizards appears optimised, not maximised.

The study concludes that TL functions as a balanced life-history trait, shaped by evolutionary trade-offs between growth, maintenance, and survival.

📉 Extremely long telomeres weren’t advantageous either. These individuals also showed reduced fitness, likely reflecting the costs of maintaining or regulating very long telomeres.

🧪 Hatchlings born with short telomeres often elongate them during juvenile growth.
But this catch-up came with a trade-off: poorer body condition later on.

✨ Key result: hatchlings with very short OR very long telomeres had lower lifetime fitness.
Those near the population mean survived longer and reproduced more.

👉 Strong evidence for stabilising selection on telomere length.

Many ectotherms keep telomerase active throughout their lifespan (unlike endotherms) 3.
Yet little is known about telomere dynamics in free-ranging animals.

💡Researchers asked: How does hatchling TL length shape lifespan and lifetime reproductive success in sand lizards?

Telomeres (TL) protect chromosome ends and maintain genome integrity, but their length is linked to disease 1,2:

• Too short → ageing-related diseases
• Too long → proliferative disorders

👉 Telomeres are elongated by the enzyme telomerase.

Is Telomere Length Optimized in Hatchling Sand Lizards? The graphical abstract image depicts the complex interplay of factors driving telomere dynamics (with permission from Dr. Chris Friesen).

🦎🧬 New in Evolution & Development: “Is Telomere Length Optimized in Hatchling Sand Lizards?”

Read below 👇

DOI: doi.org/10.1111/ede....

#Telomeres #Evolution #Ecology #Reptiles #Aging #Science #Genomics #MolecularBiology

Bibliography:

📖 Numbers correspond to the citations in the original paper. Full references omitted for brevity.

🧩 These experiments show that the epigenetic state of a single gene in engram cells can control memory—reversibly. Similar approaches could help study epigenetically influenced memories, such as those involved in childhood trauma, drug-related experiences, or neurodegeneration.

Therefore, the same epigenetic editing of Arc could enhance or suppress memory even days after learning, when memories are normally consolidated and less flexible.

🔄🧠 This shows that memory expression can be bidirectionally modulated via specific epigenetic edits.

⬆️ Activating Arc with dCas9-VPR improved memory formation and increased H3K27ac and H3K14ac at the promoter.

AcrIIA4 (anti-CRISPR protein) could block this during a second recall: animals without it kept enhanced memory, while induction reverted it.

Using c-Fos tagging and CRISPR-dCas9 tools, they targeted the Arc promoter, an immediate-early gene critical for learning and synaptic plasticity.

⬇️ Repressing Arc with dCas9-KRAB-MeCP2 led to reduced memory formation and decreased H3K27ac—a histone mark of active promoters—at the Arc promoter.

Most studies used whole-tissue assays or broad neuron populations 10-14.

❓💡The authors asked: Is the epigenetic state of a single promoter in engram cells enough to turn a memory on or off?

🧠🧩 Memory formation has been linked to epigenetic marks, mainly histone acetylation and DNA methylation 9. A sparse neuronal population called the engram is considered the physical substrate of memory 15-17 and also undergoes epigenetic modifications 18.

Cell-type- and locus-specific epigenetic editing of memory expression - Nature Genetics CRISPR-based epigenetic editing is used in a cell-type-specific, locus-restricted and temporally controllable manner in the adult mouse brain to modulate memory expression.

🚨🧬 New in Nat Genetics: “Cell-type- and locus-specific epigenetic editing of memory expression”.

Read below 👇

DOI: doi.org/10.1038/s415...

#Neuroscience #Epigenetics #Memory #BrainResearch #CRISPR #dCas9 #Science #Genomics

Side view of a transgenic zebrafish embryo that expresses a fluorescent protein that marks the the vasculature and hatching gland (magenta). In green marks the muscle, eye and parts of the brain. For more info, see ($) https://www.nature.com/articles/s41556-021-00784-w

One-day-old transgenic zebrafish embryo. Credit to Dr. Kazuhide Shaun Okuda. #ZebrafishZunday 🧪

Bibliography:

📖 Numbers correspond to the citations in the original paper. Full references omitted for brevity.

🌱💡 Take-home message:
Microbiome components can shape host phenotypes and be subject to natural selection independently of host genome changes.
Thus, microbiome can act as a non-nuclear mechanism contributing to adaptation to environmental changes.

Tryptophan metabolism links gut microbes to brain function⁶⁷ via AhR signaling⁶⁸–⁷⁰, affecting the CNS⁷¹–⁷².
🐝Lactobacillus is associated with behavior⁵⁶–⁵⁸,⁷³–⁷⁵ and memory in bees⁷⁶.
Their data suggest that Lactobacillus → tryptophan metabolism → ILA modulates activity behavior⁷⁷.

🧠 Results:

Selection on low-activity donors + microbiome transference:

⬇️ Mice locomotor activity over generations
⬇️ Lactobacillus spp. and circulating ILA

Follow-up tests show that Lactobacillus johnsonii and ILA independently reduce activity, recapitulating the selected-line phenotype⁷⁹.

🧪 What they did:

They applied selection on a behavioral trait (low activity) and transferred the gut microbiome to germ-free mice over multiple “generations” via fecal transmission through coprophagy, thereby studying microbiome-mediated host traits independently of host genetic changes.

Same genotype ≠ same phenotype when microbes differ in aphids⁹–¹². In vertebrates, can microbiomes generate phenotypic variation subject to natural selection?¹³,¹⁴ Many gut-microbes are inherited vertically in primates and other vertebrates²⁹–³¹, with long-term codiversification³²–³⁵.

🦠 Host-associated microbiomes can influence host development, ecological niches, and even evolutionary trajectories¹–⁷. However, teasing host-genetic vs microbial effects is a challenging matter.

Selection and transmission of the gut microbiome alone can shift mammalian behavior - Nature Communications Here, the authors present evidence that the gut microbiome alone, without changes in the host genome, can shape how animals respond to selection, identifying a bacterium and its metabolite that indepe...

🚨✨ New paper: “Selection and transmission of the gut microbiome alone can shift mammalian behaviour”.

DOI: doi.org/10.1038/s414...

Read below 👇

#Microbiome #Evolution #MouseModel #Behavior #Neurobiology #EvoDevo #Neuroscience

Meis2 is a transcriptional factor involved in neurodevelopment. This paper characterises its distribution in the developing brain of Xenopus leavis. Check it out!

4. Choe SK et al. 2014, Dev Cell 28:203–211, doi.org/10.1016/j.de...
5. Giliberti A et al. 2020, Eur J Med Genet 63:103627, doi.org/10.1016/j.ej...

Bibliography:

1. Agoston Z et al. 2012, BMC Dev Biol 12:10, doi.org/10.1186/1471...
2. Agoston Z et al. 2014, Development 141:28–38, doi.org/10.1242/dev....
3. Choe SK et al. 2009, Dev Cell 17:561–567, doi.org/10.1016/j.de...

📚 Meis2 is an evolutionarily conserved architect of the vertebrate brain — orchestrating regional patterning, neuronal differentiation, and circuit assembly. Its persistence in the hindbrain underscores its key role in development, evolution, and potential therapy for neurodevelopmental disorders.

🔬 Beyond this difference, Meis2 preserves its expression across the hypothalamus, optic tectum, cerebellar nuclei, and hindbrain rhombomeres (r1–r3), revealing a conserved molecular blueprint shaping vertebrate brain evolution.