HUADE INSIGHTS | Does the Chicken Embryo Really "Hear" the EGF Signal?

Does the Chicken Embryo Really "Hear" the EGF Signal?

Reference 

Kim E, Akhtar N, Li J, et al. In ovo feeding of epidermal growth factor: embryonic expression of intestinal epidermal growth factor receptor and posthatch growth performance and intestinal development in broiler chickens. Poultry Science, 2020, 99: 5736–5743. 

Statement

This article is a translated and condensed summary based on the above review article. The content has been reorganized for scientific communication and educational purposes and does not represent the complete views of the original publication. Readers are encouraged to consult the original article for comprehensive information.

In our previous article, we mentioned that scientists hope to use in ovo feeding to promote intestinal development in chickens before they even hatch. This idea sounds reasonable — if EGF can act at the most critical stage of intestinal development, it should, in theory, help chicks establish a healthy digestive system more quickly.

But here's the question: can the chicken embryo actually "receive" the growth signal sent out by EGF? This is the first question the entire experiment needed to answer. Rather than rushing to measure body weight or immediately check the feed-to-meat ratio, the researchers first did something basic but crucial — they looked at whether the EGF receptor (EGFR) in the intestine showed any response. The logic is simple: any growth factor is like a letter that has been mailed, and the receptor is the recipient. If there is no receptor, or if the receptor doesn't respond, then no matter how good the growth factor is, it cannot take effect. So before evaluating whether EGF is useful, it was first necessary to confirm whether the chicken embryo had actually "heard" this signal at all.





For Four Straight Days, Almost Nothing Happened

To answer this question, the research team injected different doses of EGF into the amniotic cavity on day 17 of incubation, then measured changes in EGFR gene expression in the embryonic jejunum tissue every day from day 17 through day 21 (the day of hatching).

The researchers originally expected that if EGF was having an effect, changes in receptor expression should appear fairly quickly. But the experimental results were somewhat unexpected — for four consecutive days, from day 17 to day 20, there was no significant difference in EGFR expression levels between the EGF-treated groups and the control group. It was not until day 21, right as the chicks were about to hatch, that the change suddenly appeared: EGFR expression levels in both the 160 μg/kg and 640 μg/kg EGF-treated groups were significantly higher than in the control group, reaching as much as 4 to 5 times the control level at the peak.

In other words, EGF was not going "unheard" — the response simply came much later than anyone had expected.

Why did this happen? The paper's authors proposed an explanation worth paying attention to: during the early stages of embryonic development, although EGFR had already begun to be expressed, the intestinal cells themselves were not yet fully mature. In other words, it wasn't that EGF failed to send out its signal — it was that the cells weren't yet ready to receive it. As the embryo gradually matured, more and more cells became capable of responding to EGF, and receptor expression rose rapidly as a result. This suggests that for EGF to truly take effect, it requires not just the signal itself, but also cells that have developed the capacity to "receive" that signal — much like a conference call where one party has already started speaking, but the other hasn't joined yet. Real communication only begins once everyone has entered the meeting room.



Dose More Than Quadrupled, But the Response Didn't Follow

Another detail is equally worth noting. The study set up two dosage levels: 160 μg/kg and 640 μg/kg. In theory, the higher dose should have produced a stronger response, but the experimental results showed no clear difference between the two — increasing the dose did not lead to a corresponding increase in receptor expression. This suggests that for growth factors like EGF, "more is not necessarily better" — the cell's own capacity to respond is governed by its own regulatory mechanisms.

Up to this point, the story seems to be heading in a positive direction — EGF entered the chicken embryo, and the receptor did indeed respond. By ordinary logic, one would expect the chicks' subsequent growth performance and intestinal development to be better than in the control group. However, the truly surprising twist happens right here: after the research team continued raising the chicks for 21 days, they found that almost none of the production performance indicators showed a statistically significant improvement. The signal had appeared, but the results did not follow — and it is precisely this contrast that the next article will explore in depth.



HUADE Technical Perspective

The greatest value of this experiment is not that it proves EGF is "effective" or "ineffective" — it first answers a more fundamental question: the chicken embryo is able to recognize the EGF signal. For R&D purposes, this means that a real, genuine target exists. But moving from the laboratory to actual production requires far more than simply identifying a target. What truly determines whether a technology can be successfully implemented is usually not "whether a signal exists," but whether that signal can be consistently and stably translated into real gains in animal production performance. This is a hurdle that every functional bioactive substance must clear during development — and it is a principle that applies equally whenever we evaluate any raw material in practice.