Justin Blumenstiel

@bdelloid.bsky.social

Evolution, Genomics, Genetics, Epigenetics, Transposons, Small RNAs, Meiosis, Politics, Music, Kansas....AND DROSOPHILA!!! Freaked out ribosome and DNA truther doing my own research. "We are our own reviewers" - Alejandro Montenegro‬ ‪

In addition to the ways that genome defense has been recruited for host function, a number of other mechanisms of immunity have been also
recruited in a developmental context. If the ancestral function of RNA silencing was for immunity (See Box 1, but also see [155]), then
developmental regulation by miRNAs represents a striking example of adaptation derived from an immune module. But there are a number of
additional examples whereby immune function has been repurposed for development. Proteins carrying Toll/interleukin-1/resistance gene
(TIR) domains play a role in immunity signaling across animals, plants and bacteria, suggesting an ancestral immune function [156–159]. This
ancestral function has subsequently been repurposed in Toll-like receptors for a variety of developmental functions in flies [160], nematodes
[161], sea anemone [162] and also in mammals.. Another
example of immune function repurposing is provided by the process of synaptic pruning mediated by the complement cascade protein C1q. ...In the developing brain, synaptic pruning of excess or weak synapses is critical for proper neuronal connectivity and complement
cascade protein C1q has been shown to trigger synapse elimination via engulfment by microglia, ..
Why might immune function be frequently repurposed for development? I propose two reasons. First, the logic of immunity, which targets
suppression based on information about the target (i.e, self vs non-self), can be inherently useful for targeted suppression of gene expression or
cell-type. ... A second reason that immune systems may be frequently repurposed is based
on an evolvability argument. It seems reasonable that, from a fitness perspective, pathogens are a (the?) primary challenge for living organisms.
For this reason,..speculatively, I propose that evolution of immune or defense systems would be a primary requirement and that
developmental refinement of form would be a secondary target for natural selection during early evolution

Wait, wut?
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Christ almighty. Head back.

Communion book by Whitley Streier cover. With classic alien.

#Nokings protest in Lawrence, KS. March 28, 2026

No Kings Protest. #nokings. Me holding a sign saying "Stop the Mad King"

Rudy Renfer LinkedIn: About
My experience has provided me a sound analytical ability, excellent communication skills, the ability to accurately and precisely articulate the critical issues in a case, superior oral and writing skills, exceptional research skills, interpersonal skills, and sound judgment. In my extensive experience as a criminal and civil attorney, I have overseen investigations, documented investigations, deciphered complex factual scenarios, conducted witness interviews and depositions, coordinated with various client agencies, and advised investigators how to conduct interviews. I also have extensive jury trial experience.

Guy waiting in swinging chair, at desk, in empty pool.

No more copy-pasting
Forget switching between ChatGPT and your LMS. Einstein reads the assignment, solves it, and submits it directly.

Locked arms meme. Mutation rate. Population Size. Theta

Natalie Portman meme.
Panel 1: Check out this amazing correlation.
Panel 2: You controlled for phylogeny, right?
Panel 3: Blank stare.
Panel 4: Right

Submitted: December 3, 2025
Published: November 13, 2025

$In his 1972 paper, "Fisher's ‘fundamental theorem’ made clear," George Price provided the rigorous mathematical proof that Fisher’s theorem was not an approximation, but an exact statement—provided one understands that Fisher was only talking about the "partial change" in fitness.The Exact QuotePrice clarifies the distinction between the total change in fitness and the specific component Fisher was measuring:"The theorem characterizes the partial change in the average fitness of a population that is directly ascribed to the action of natural selection... it does not give the total change in average fitness. This total change is the sum of two parts: a part due to natural selection (which is the part Fisher’s theorem is about) and a part due to 'environmental change'."The Price Equation ContextPrice demonstrated that the total change in mean fitness ($\Delta \bar{w}$) can be partitioned into two distinct terms. This is often represented conceptually as:$$\Delta \bar{w} = \text{Cov}(w_i, z_i) + E(w_i, \Delta z_i)$$The first term ($\text{Cov}$): This represents the Fisherian part. It is the change in the trait (fitness) due to the covariance between the trait and fitness (selection). For fitness itself, this covariance equals the additive genetic variance ($V_A$).The second term ($E$): This represents the "Environmental" part. In this context, "environment" includes everything that changes the relationship between genes and fitness from one generation to the next—including dominance, epistasis, and external environmental shifts.Why this explains your discrepancyIn your calculation, when you used $\Delta p$ to find the new mean fitness, you were calculating the Total Change.When you used $V_A$, you were calculating only the Partial Change.$

$. Comparing the Two ResultsPrediction from $V_A$ (Fisher): $\Delta \bar{w} = 0.000789439$Actual $\Delta \bar{w}$ (from $\Delta p$): $1.00082435 - 1.0 = \mathbf{0.00082435}$Why are they different?You likely noticed that the actual change ($0.000824$) is slightly higher than the Fisher prediction ($0.000789$). This is a classic "aha!" moment in quantitative genetics:Linear Approximation: Fisher's Theorem is a first-order derivative. It predicts the change in fitness based on the current state of the population. It assumes the "slope" of the fitness increase stays constant.The "Moving" Population: In reality, as $p$ increases, the population becomes slightly more efficient at producing the $A_1A_1$ genotype in the very next generation than the linear prediction accounts for.Non-Zero Higher Moments: Fisher’s theorem technically states that the rate of change is equal to the $V_A$, but it doesn't account for the change in $V_A$ itself as the frequency shifts within that same generation.In your specific case, the discrepancy is small because $p$ is small. If $p$ were $0.5$, the "gap" between the Fisher prediction and the actual change would be more pronounced.$