In short, they edited mice to have Foxp2 deleted in only specific regions of the brain, one of them being striatum. But those mice didn’t have the ‘speech’ defects that mice with whole-body Foxp2 knock-outs showed. So Foxp2′s action outside of the striatum seems to play a role. They didn’t do a striatum+cerebellum knock-out, though, so it could still be those two jointly (but not individually) causing the problem.
That paper repeatedly does the annoyingly-common thing of conflating “our tests didn’t find any group differences that pass the p<0.05 threshold” with “our tests positively confirm that there are no group differences”. 😠 I’m not saying they’re necessarily wrong about that, I’m just complaining.
No, actually, I will complain, and they are wrong. Their tests show that, in global knockouts (well, “spontaneous deletion”, but I think it amounts to the same thing?), ultrasonic vocalizations (USV) go significantly down while “click” vocalizations go significantly up. So at that point, one would think that they should do 1-sided t-tests on the region-specific knockouts to see if USVs go down and if clicks go up. But instead they did 1-sided tests to see if USVs go down and if clicks go down. And the clicks actually went up (who would have guessed!), which they reported as “click rates [were not] affected [with] p=0.99”. 🤦🤦🤦
I guess that they were trying to avoid p-hacking by pre-committing to which tests they’d run, which I suppose is admirable, but I still think they were being pretty boneheaded here!! (Unless I misunderstand. I was skimming.)
Anyway, the USV result does indeed look like “no change”, but clicks went up (with “p=0.99” on the incorrectly-oriented 1-sided t-test, which really means p=0.01) for both the Purkinje- & striatum-specific knockouts. (Not cortex.)
That still leaves the USV question. The hypothesis that FOXP2 impacts USV squeaking in mice via the lungs still seems to me like a live possibility, in which case FOXP2→mouse-USV-squeaking would be totally disanalogous to FOXP2→human-speech, I think, i.e. just a funny coincidence. Hmm. The striatum+cerebellum interaction thing you mentioned is also possible AFAIK.
(I have somewhat more confidence that FOXP2-affects-bird-vocalization ↔ FOXP2-affects-human speech is mechanistically analogous, than that FOXP2-affects-mouse-vocalization ↔ FOXP2-affects-human speech is mechanistically analogous. I think the human-vs-bird symptoms are more closely related, not just “hey in both cases it has something to do with vocalizations”. This might be wrong though, I didn’t double-check.)
Human speech and bird song are both cases of vocal learning. They are (at least) largely learned, more complex and require more precision control, whereas mouse vocalizations are mostly hardwired
https://en.wikipedia.org/wiki/Vocal_learning?wprov=sfla1
Sounds plausible but this article is evidence against the striatum hypothesis: Region-specific Foxp2 deletions in cortex, striatum or cerebellum cannot explain vocalization deficits observed in spontaneous global knockouts
In short, they edited mice to have Foxp2 deleted in only specific regions of the brain, one of them being striatum. But those mice didn’t have the ‘speech’ defects that mice with whole-body Foxp2 knock-outs showed. So Foxp2′s action outside of the striatum seems to play a role. They didn’t do a striatum+cerebellum knock-out, though, so it could still be those two jointly (but not individually) causing the problem.
Interesting!!
That paper repeatedly does the annoyingly-common thing of conflating “our tests didn’t find any group differences that pass the p<0.05 threshold” with “our tests positively confirm that there are no group differences”. 😠 I’m not saying they’re necessarily wrong about that, I’m just complaining.
No, actually, I will complain, and they are wrong. Their tests show that, in global knockouts (well, “spontaneous deletion”, but I think it amounts to the same thing?), ultrasonic vocalizations (USV) go significantly down while “click” vocalizations go significantly up. So at that point, one would think that they should do 1-sided t-tests on the region-specific knockouts to see if USVs go down and if clicks go up. But instead they did 1-sided tests to see if USVs go down and if clicks go down. And the clicks actually went up (who would have guessed!), which they reported as “click rates [were not] affected [with] p=0.99”. 🤦🤦🤦
I guess that they were trying to avoid p-hacking by pre-committing to which tests they’d run, which I suppose is admirable, but I still think they were being pretty boneheaded here!! (Unless I misunderstand. I was skimming.)
Anyway, the USV result does indeed look like “no change”, but clicks went up (with “p=0.99” on the incorrectly-oriented 1-sided t-test, which really means p=0.01) for both the Purkinje- & striatum-specific knockouts. (Not cortex.)
That still leaves the USV question. The hypothesis that FOXP2 impacts USV squeaking in mice via the lungs still seems to me like a live possibility, in which case FOXP2→mouse-USV-squeaking would be totally disanalogous to FOXP2→human-speech, I think, i.e. just a funny coincidence. Hmm. The striatum+cerebellum interaction thing you mentioned is also possible AFAIK.
(I have somewhat more confidence that FOXP2-affects-bird-vocalization ↔ FOXP2-affects-human speech is mechanistically analogous, than that FOXP2-affects-mouse-vocalization ↔ FOXP2-affects-human speech is mechanistically analogous. I think the human-vs-bird symptoms are more closely related, not just “hey in both cases it has something to do with vocalizations”. This might be wrong though, I didn’t double-check.)
Human speech and bird song are both cases of vocal learning. They are (at least) largely learned, more complex and require more precision control, whereas mouse vocalizations are mostly hardwired https://en.wikipedia.org/wiki/Vocal_learning?wprov=sfla1