Fig 3. MOs-c PT and CT are required for the progression and coordination of RWD.

a. Photoinhibition mapping of cortical areas by closed-loop activation of inhibitory interneurons. Inactivation of the contralateral areas of MOs-c (1), MOp-ul (2), and SSp-ul (4) decreased supination probability. Color scale represents changes in success probability between inhibition and control trials. ($n=5$ Pvalb;Ai32 mice, see Supplementary Table 1 for statistics)

b. Perturbation of movement progression upon close-loop MOs-c inactivation during reach in an example control and inhibition movement trajectory. In the inhibition trial, the reach was aborted; the hand returned to the start position, followed by another failed attempt.

c. Impaired action sequence progression in control (left) and inhibition (right) trials upon contralateral MOs-c inhibition. 18% (81/441) control trials and 63% (209/331) inhibition trials failed to complete the RWD sequence. ($n=5$ Pvalb;Ai32 mice)

d. Effects of prolonged inhibition of PN types by expressing optogenetic inhibitory opsins in MOs-c (turquoise). Heatmap summarized the change in success probability of action phases upon prolonged inhibition of each PN type compared with control trials. Same mice for all following panels. ($n=15$ sessions from 8 PN^Emx1 mice; 8 sessions from 6 IT^Cux1 mice; 12 sessions from 7 IT^PlxnD1 mice; 13 sessions from 7 PT^Fezf2 mice; 11 sessions from 6 CT^Tle4 mice.)

e. Reduction of reach and withdraw success probability with prolonged PN^Emx1 inhibition. Reach was quantified as target contact probability from all trials with successful lifts (two-sample Kolmogorov-Smirnov (KS) test, KS distance $\left(d\right)=0.72,p=3.20\times {10}^{-24}$). Withdraw was quantified as supination probability with successful reach (Wilcoxon rank sum test, $\mathrm{*}\mathrm{*}p<0.01$).

f. Coherent hand-mouth movement time series during drinking. Hand upward position, digit open size, mouth open area, and lick onset variables are indicated.

g. Increased premature lick probability during PN^Emx1 inhibition ($n=15$, Wilcoxon rank sum test, $\mathrm{*}\mathrm{*}p<$ $0.01$).

h. Increased variance in hand position relative to the mouth upon the onset of hand lick during PN^Emx1 inhibition ($n=15$, Wilcoxon rank sum test, $p<0.001$).

i. Abnormal hand posture during drinking with prolonged PN^Emx1 inhibition indicated by palm-facing direction at lick onset ($n=13734$ control and 9186 inhibition licks, two-sample KS test, $d=0.20,p=$ $1.61\times {10}^{-202}$).

j. Schematic of the prolonged inhibition of MOs-c PN types.

k. PT ^Fezf2 and CT^Tle4 inhibition on success probability of reach and withdraw. Left: ANOVA; PT^Fezf2 inhibition $F_{\mathrm{1,56}}=11.52,\mathrm{*}\mathrm{*}p=0.0053;{\mathrm{C}\mathrm{T}}^{\mathrm{T}\mathrm{l}\mathrm{e}4}$ inhibition $F_{\mathrm{1,40}}=10.82,\mathrm{*}\mathrm{*}p=0.0082$. Note the target location-dependent impairment in PT^Fezf2 (inhibition × target $F_{\mathrm{4,56}}=4.41,p=0.0041$) but not in CT^Tle4 (inhibition × target $F_{\mathrm{4,40}}=0.51,p=0.7280$). Right: Wilcoxon rank sum test, $\mathrm{*}\mathrm{*}\mathrm{*}p<0.001$.

l. Variance in hand position (left) and hand posture (right) during PT ^Fezf2 and CT^Tle4 inhibition. (Left: Wilcoxon rank sum test, $\mathrm{*}\mathrm{*}p<0.01$. Right: two-sample KS test, $\mathrm{*}\mathrm{*}\mathrm{*}p<0.001$.)