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An evolutionary role for acquired adjustments, including learning, in allowing persistence and changing the natural selection experienced by inherited variants. It does not require direct inheritance of learned contents.
Recovery of a declining biological population through inherited adaptive change. Immediate survival enabled by phenotypic plasticity can provide time for rescue, but is not itself evidence that inherited rescue occurred.
Resemblance between organisms that influences a receiver’s animal behaviour and thereby changes fitness. Similarity alone does not establish the receiver-mediated evolutionary process.
Reproductive contribution measured relative to a specified population, environment and timescale. Survival or task performance is a component or proxy, not automatically total reproductive success.
Gene loss is evolutionary loss or functional inactivation of an inherited gene. A lineage can lose a function that has become unnecessary, obtain its product from a partner, or retain an alternative pathway. Losing a required function can instead be harmful; absence alone does not establish adaptation.
Comparative evidence must distinguish a true loss from incomplete genome assembly or a sequence that has diverged beyond recognition. Repeated joint losses of EDS1, PAD4 and associated plant immunity components illustrate how loss can reveal dependence within an interacting pathway.[ref]
EDS1 and PAD4 pathway-loss study by Erin L. Baggs and others. Abstract: convergent pathway loss
Change among cell lineages within an organism through mutation, drift and selection. Success of a cell lineage can conflict with the reproductive success of the organism.
A transition in which previously reproducing entities become integrated into a new higher-level reproductive unit. cooperation and control of lower-level conflict are complementary issues.
Differential expansion or persistence of lineages under a specified environment. Increased survival can confer an advantage even without a higher instantaneous division rate.
A family of hypotheses concerning continuing adaptation in response to other evolving organisms. In explanations of sex, changing host-parasite associations can favour production of less familiar host genotypes; the advantage is conditional.
Loss of an inherited anatomical or molecular feature. Its inference requires distinguishing genuine absence from incomplete observation and reconstructing the ancestral state.
Some ribonucleases cut internal phosphodiester bonds, whereas others remove nucleotides from an end. Selective RNA degradation contributes to processing and regulation, so cleavage can produce a functional mature RNA as well as destroy a transcript. [ref]
Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. Chapters 3, 6 and 15, protein function, translation and cell signalling
A nuclease is an enzyme that cleaves nucleic acids. ribonucleases act on RNA; other activities act on DNA. Nuclease sensitivity can reveal a nucleic-acid-dependent assembly, but loss of association can also reflect secondary structural disruption.
dihydrofolate reductase catalyzes reduction of dihydrofolate to tetrahydrofolate using NADPH. Its catalytic cycle is a model for connecting protein dynamics, binding and release.[ref]
The dynamic energy landscape of dihydrofolate reductase catalysis by David D. Boehr and others. pp. 1638–1642, dynamic states across the catalytic cycle
A recombinase is an enzyme that catalyzes a genetic recombination reaction. The RecA family performs homology-dependent DNA strand exchange; the term also includes enzymes with other recombination mechanisms.
An enzyme that changes nucleic-acid topology by transient strand cleavage and resealing. Activity on DNA can change DNA supercoiling.
An enzyme that adds methyl groups to specified histone residues. Its presence alone does not specify repression, because distinct modified sites can have different regulatory roles.
An enzyme that removes acetyl groups from histones. Its local recruitment can oppose histone acetylation and favor repressive chromatin.
Pinned article: Introduction to the OurBigBook Project
Welcome to the OurBigBook Project! Our goal is to create the perfect publishing platform for STEM subjects, and get university-level students to write the best free STEM tutorials ever.
Everyone is welcome to create an account and play with the site: ourbigbook.com/go/register. We belive that students themselves can write amazing tutorials, but teachers are welcome too. You can write about anything you want, it doesn't have to be STEM or even educational. Silly test content is very welcome and you won't be penalized in any way. Just keep it legal!
Intro to OurBigBook
. Source. We have two killer features:
- topics: topics group articles by different users with the same title, e.g. here is the topic for the "Fundamental Theorem of Calculus" ourbigbook.com/go/topic/fundamental-theorem-of-calculusArticles of different users are sorted by upvote within each article page. This feature is a bit like:
- a Wikipedia where each user can have their own version of each article
- a Q&A website like Stack Overflow, where multiple people can give their views on a given topic, and the best ones are sorted by upvote. Except you don't need to wait for someone to ask first, and any topic goes, no matter how narrow or broad
This feature makes it possible for readers to find better explanations of any topic created by other writers. And it allows writers to create an explanation in a place that readers might actually find it.
Figure 1. Screenshot of the "Derivative" topic page. View it live at: ourbigbook.com/go/topic/derivativeVideo 2. OurBigBook Web topics demo. Source. - local editing: you can store all your personal knowledge base content locally in a plaintext markup format that can be edited locally and published either:This way you can be sure that even if OurBigBook.com were to go down one day (which we have no plans to do as it is quite cheap to host!), your content will still be perfectly readable as a static site.
- to OurBigBook.com to get awesome multi-user features like topics and likes
- as HTML files to a static website, which you can host yourself for free on many external providers like GitHub Pages, and remain in full control
Figure 2. You can publish local OurBigBook lightweight markup files to either OurBigBook.com or as a static website.
Figure 3. Visual Studio Code extension installation.
Figure 5. . You can also edit articles on the Web editor without installing anything locally. Video 3. Edit locally and publish demo. Source. This shows editing OurBigBook Markup and publishing it using the Visual Studio Code extension. 
- Infinitely deep tables of contents:
All our software is open source and hosted at: github.com/ourbigbook/ourbigbook
Further documentation can be found at: docs.ourbigbook.com
Feel free to reach our to us for any help or suggestions: docs.ourbigbook.com/#contact