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Shox2 is required for the proper development of the facial motor nucleus and the establishment of the facial nerves.

Rosin JM, Kurrasch DM, Cobb J - BMC Neurosci (2015)

Bottom Line: Using a Nestin-Cre driver, we show that elimination of Shox2 throughout the brain results in elevated cell death in the facial motor nucleus at embryonic day 12.5 (E12.5) and E14.5, which correlates with impaired axonal projection properties of vMNs.We also observed changes in the spatial expression of the vMN cell fate factors Isl1 and Phox2b, and concomitant defects in Shh and Ptch1 expression in Shox2 mutants.Furthermore, we demonstrate that elimination of Shox2 results in the loss of dorsomedial and ventromedial subnuclei by postnatal day 0 (P0), which may explain the changes in physical activity and impaired feeding/nursing behavior in Shox2 mutants.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., BI286D, Calgary, AB, T2N 1N4, Canada. jmrosin2013@gmail.com.

ABSTRACT

Background: Axons from the visceral motor neurons (vMNs) project from nuclei in the hindbrain to innervate autonomic ganglia and branchial arch-derived muscles. Although much is known about the events that govern specification of somatic motor neurons, the genetic pathways responsible for the development of vMNs are less well characterized. We know that vMNs, like all motor neurons, depend on sonic hedgehog signaling for their generation. Similarly, the paired-like homeobox 2b (Phox2b) gene, which is expressed in both proliferating progenitors and post-mitotic motor neurons, is essential for the development of vMNs. Given that our previous study identified a novel role for the short stature homeobox 2 (Shox2) gene in the hindbrain, and since SHOX2 has been shown to regulate transcription of islet 1 (Isl1), an important regulator of vMN development, we sought to determine whether Shox2 is required for the proper development of the facial motor nucleus.

Results: Using a Nestin-Cre driver, we show that elimination of Shox2 throughout the brain results in elevated cell death in the facial motor nucleus at embryonic day 12.5 (E12.5) and E14.5, which correlates with impaired axonal projection properties of vMNs. We also observed changes in the spatial expression of the vMN cell fate factors Isl1 and Phox2b, and concomitant defects in Shh and Ptch1 expression in Shox2 mutants. Furthermore, we demonstrate that elimination of Shox2 results in the loss of dorsomedial and ventromedial subnuclei by postnatal day 0 (P0), which may explain the changes in physical activity and impaired feeding/nursing behavior in Shox2 mutants.

Conclusions: Combined, our data show that Shox2 is required for development of the facial motor nucleus and its associated facial (VII) nerves, and serves as a new molecular tool to probe the genetic programs of this understudied hindbrain region.

No MeSH data available.


Related in: MedlinePlus

Nestin-Cre driven conditional Shox2-deletion results in disruptions in the facial motor nucleus and changes in cell death. a, b Ventral view of the P0 brain of control (a) and Nestin-Cre; Shox2flox/− (b) animals stained with the 2H3 antibody demonstrate that the facial motor nucleus (nVII) is severely reduced in Nestin-Cre; Shox2flox/− pups (compare a to b, dashed-circle and arrows). c–f X-gal staining of P0 control (c, e) and Nestin-Cre; Shox2lacZ/flox (d, f) pup brains (viewed ventrally) show Shox2 expression in the facial motor nucleus and demonstrate that the nucleus is severely reduced in size (compare e to f, arrows) in mice lacking Shox2 function. Cleaved active-CASP3 immunostaining on E12.5 (g, h), E14.5 (j, k), E16.5 (m, n) and P0 (p, q) control (g, j, m, p) and Nestin-Cre; Shox2flox/− mutant (h, k, n, q) sagittal sections through the facial motor nucleus (nVII). i Quantification of the number of cleaved active-CASP3 + cells present in the E12.5 facial motor nucleus (see g, h) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0038). l Quantification of the number of cleaved active-CASP3 + cells present in the E14.5 facial motor nucleus (see j, k) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). o Quantification of the number of cleaved active-CASP3 + cells present in the E16.5 facial motor nucleus (see m, n) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.1929). r Quantification of the number of cleaved active-CASP3 + cells present in the P0 facial motor nucleus (see p, q, dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.6875). s Quantification of the number of cleaved active-CASP3 + cells present in and around the P0 facial motor nucleus (see p, q, entire panel including cells within the dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). t, u Representative binary particle area diagrams from ImageJ displaying Shox2lacZ + cell staining at E14.5 (t) and P0 (u) in controls and NestinCre; Shox2lacZ/flox facial motor nuclei. v Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the E14.5 facial motor nucleus (see t) of control and Nestin-Cre; Shox2lacZ/flox embryos (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0027). w Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the P0 facial motor nucleus (see u) of control and Nestin-Cre; Shox2lacZ/flox animals (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0011). cb cerebellum. a–fScale bar 500 μm. g–qScale bar 250 μm.
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Fig4: Nestin-Cre driven conditional Shox2-deletion results in disruptions in the facial motor nucleus and changes in cell death. a, b Ventral view of the P0 brain of control (a) and Nestin-Cre; Shox2flox/− (b) animals stained with the 2H3 antibody demonstrate that the facial motor nucleus (nVII) is severely reduced in Nestin-Cre; Shox2flox/− pups (compare a to b, dashed-circle and arrows). c–f X-gal staining of P0 control (c, e) and Nestin-Cre; Shox2lacZ/flox (d, f) pup brains (viewed ventrally) show Shox2 expression in the facial motor nucleus and demonstrate that the nucleus is severely reduced in size (compare e to f, arrows) in mice lacking Shox2 function. Cleaved active-CASP3 immunostaining on E12.5 (g, h), E14.5 (j, k), E16.5 (m, n) and P0 (p, q) control (g, j, m, p) and Nestin-Cre; Shox2flox/− mutant (h, k, n, q) sagittal sections through the facial motor nucleus (nVII). i Quantification of the number of cleaved active-CASP3 + cells present in the E12.5 facial motor nucleus (see g, h) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0038). l Quantification of the number of cleaved active-CASP3 + cells present in the E14.5 facial motor nucleus (see j, k) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). o Quantification of the number of cleaved active-CASP3 + cells present in the E16.5 facial motor nucleus (see m, n) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.1929). r Quantification of the number of cleaved active-CASP3 + cells present in the P0 facial motor nucleus (see p, q, dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.6875). s Quantification of the number of cleaved active-CASP3 + cells present in and around the P0 facial motor nucleus (see p, q, entire panel including cells within the dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). t, u Representative binary particle area diagrams from ImageJ displaying Shox2lacZ + cell staining at E14.5 (t) and P0 (u) in controls and NestinCre; Shox2lacZ/flox facial motor nuclei. v Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the E14.5 facial motor nucleus (see t) of control and Nestin-Cre; Shox2lacZ/flox embryos (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0027). w Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the P0 facial motor nucleus (see u) of control and Nestin-Cre; Shox2lacZ/flox animals (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0011). cb cerebellum. a–fScale bar 500 μm. g–qScale bar 250 μm.

Mentions: Since Shox2-mutant embryos and neonates display impaired axonal projection properties and were unable to nurse properly, we next wanted to determine if development of the facial motor nucleus was disrupted in the absence of Shox2. Both neurofilament and lacZ staining of P0 control and Nestin-Cre; Shox2flox/− or Nestin-Cre; Shox2lacZ/flox pup brains demonstrated that the facial motor nucleus was severely reduced in size, with disruptions in neuronal spatial organization in mice lacking Shox2 function (Figure 4a–f, arrows; note that the Shox2lacZ allele is a or severely hypomorphic allele, see “Methods”). While the symmetry between the left and right facial motor nuclei appears to be relatively maintained (Figure 4c–d, arrows), the two lobes that normally comprise the facial motor nucleus are no longer present (Figure 4e–f, arrows). We next investigated whether an increase in apoptosis could account for the changes observed in the facial motor nucleus of Shox2-mutant brains. We found an increase in the number of apoptotic cells present at E12.5 and E14.5 in the facial motor nucleus of Shox2-mutants (Figure 4g–l); however, no significant increase in apoptosis was detected in the E16.5 or P0 facial motor nucleus of Shox2-mutant animals (Figure 4m–r). We observed a ~7.5-fold increase in the number of cleaved active-CASP3 + cells in the E12.5 facial motor nucleus of Nestin-Cre; Shox2flox/− animals as compared to controls (Figure 4i; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0038). We also observed a striking ~17.7-fold increase in the number of cleaved active-CASP3 + cells in the E14.5 facial motor nucleus of Nestin-Cre; Shox2flox/− animals as compared to controls (Figure 4l; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0007). While the slight elevation in apoptosis detected in the E16.5 and P0 facial motor nucleus of Shox2-mutant animals was not significantly different from controls (Figure 4o, r), we did observe a ~3.5-fold increase in the number of cleaved active-CASP3 + cells at P0 when we included the tissue immediately surrounding the facial motor nucleus of Nestin-Cre; Shox2flox/− animals (Figure 4p–q, entire panel including cells within the dashed-circle) in our cell count (Figure 4s; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0007). Moreover, when we calculated the area of Shox2lacZ + cells remaining in sagittal sections through the center of the facial motor nucleus of Nestin-Cre; Shox2lacZ/flox animals as compared to controls at E14.5 (Figure 4t) and P0 (Figure 4u), we observed a ~44% decrease in the area of Shox2lacZ + cells in the E14.5 facial motor nucleus (Figure 4v; control n = 3, Nestin-Cre; Shox2lacZ/flox n = 3, p = 0.0027) and a ~53% decrease in the area of Shox2lacZ + cells in the P0 facial motor nucleus (Figure 4w; control n = 3, Nestin-Cre; Shox2lacZ/flox n = 3, p = 0.0011). Therefore, the higher levels of apoptosis are correlated with a decrease in the size of the facial motor nucleus, and taken together, the results demonstrate that apoptosis contributes to the disruptions observed in the facial motor nucleus of Nestin-Cre; Shox2flox/− animals.Figure 4


Shox2 is required for the proper development of the facial motor nucleus and the establishment of the facial nerves.

Rosin JM, Kurrasch DM, Cobb J - BMC Neurosci (2015)

Nestin-Cre driven conditional Shox2-deletion results in disruptions in the facial motor nucleus and changes in cell death. a, b Ventral view of the P0 brain of control (a) and Nestin-Cre; Shox2flox/− (b) animals stained with the 2H3 antibody demonstrate that the facial motor nucleus (nVII) is severely reduced in Nestin-Cre; Shox2flox/− pups (compare a to b, dashed-circle and arrows). c–f X-gal staining of P0 control (c, e) and Nestin-Cre; Shox2lacZ/flox (d, f) pup brains (viewed ventrally) show Shox2 expression in the facial motor nucleus and demonstrate that the nucleus is severely reduced in size (compare e to f, arrows) in mice lacking Shox2 function. Cleaved active-CASP3 immunostaining on E12.5 (g, h), E14.5 (j, k), E16.5 (m, n) and P0 (p, q) control (g, j, m, p) and Nestin-Cre; Shox2flox/− mutant (h, k, n, q) sagittal sections through the facial motor nucleus (nVII). i Quantification of the number of cleaved active-CASP3 + cells present in the E12.5 facial motor nucleus (see g, h) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0038). l Quantification of the number of cleaved active-CASP3 + cells present in the E14.5 facial motor nucleus (see j, k) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). o Quantification of the number of cleaved active-CASP3 + cells present in the E16.5 facial motor nucleus (see m, n) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.1929). r Quantification of the number of cleaved active-CASP3 + cells present in the P0 facial motor nucleus (see p, q, dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.6875). s Quantification of the number of cleaved active-CASP3 + cells present in and around the P0 facial motor nucleus (see p, q, entire panel including cells within the dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). t, u Representative binary particle area diagrams from ImageJ displaying Shox2lacZ + cell staining at E14.5 (t) and P0 (u) in controls and NestinCre; Shox2lacZ/flox facial motor nuclei. v Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the E14.5 facial motor nucleus (see t) of control and Nestin-Cre; Shox2lacZ/flox embryos (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0027). w Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the P0 facial motor nucleus (see u) of control and Nestin-Cre; Shox2lacZ/flox animals (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0011). cb cerebellum. a–fScale bar 500 μm. g–qScale bar 250 μm.
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Fig4: Nestin-Cre driven conditional Shox2-deletion results in disruptions in the facial motor nucleus and changes in cell death. a, b Ventral view of the P0 brain of control (a) and Nestin-Cre; Shox2flox/− (b) animals stained with the 2H3 antibody demonstrate that the facial motor nucleus (nVII) is severely reduced in Nestin-Cre; Shox2flox/− pups (compare a to b, dashed-circle and arrows). c–f X-gal staining of P0 control (c, e) and Nestin-Cre; Shox2lacZ/flox (d, f) pup brains (viewed ventrally) show Shox2 expression in the facial motor nucleus and demonstrate that the nucleus is severely reduced in size (compare e to f, arrows) in mice lacking Shox2 function. Cleaved active-CASP3 immunostaining on E12.5 (g, h), E14.5 (j, k), E16.5 (m, n) and P0 (p, q) control (g, j, m, p) and Nestin-Cre; Shox2flox/− mutant (h, k, n, q) sagittal sections through the facial motor nucleus (nVII). i Quantification of the number of cleaved active-CASP3 + cells present in the E12.5 facial motor nucleus (see g, h) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0038). l Quantification of the number of cleaved active-CASP3 + cells present in the E14.5 facial motor nucleus (see j, k) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). o Quantification of the number of cleaved active-CASP3 + cells present in the E16.5 facial motor nucleus (see m, n) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.1929). r Quantification of the number of cleaved active-CASP3 + cells present in the P0 facial motor nucleus (see p, q, dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.6875). s Quantification of the number of cleaved active-CASP3 + cells present in and around the P0 facial motor nucleus (see p, q, entire panel including cells within the dashed-circle) of control and Nestin-Cre; Shox2flox/− embryos (plotted values are the mean ± S.E.M, 3 sections per animals, n = 3 animals, p = 0.0007). t, u Representative binary particle area diagrams from ImageJ displaying Shox2lacZ + cell staining at E14.5 (t) and P0 (u) in controls and NestinCre; Shox2lacZ/flox facial motor nuclei. v Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the E14.5 facial motor nucleus (see t) of control and Nestin-Cre; Shox2lacZ/flox embryos (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0027). w Quantification of the area of Shox2lacZ + cells present in sagittal sections through the center of the P0 facial motor nucleus (see u) of control and Nestin-Cre; Shox2lacZ/flox animals (plotted values are the mean ± S.E.M, control = 3, Nestin-Cre; Shox2lacZ/flox = 3, p = 0.0011). cb cerebellum. a–fScale bar 500 μm. g–qScale bar 250 μm.
Mentions: Since Shox2-mutant embryos and neonates display impaired axonal projection properties and were unable to nurse properly, we next wanted to determine if development of the facial motor nucleus was disrupted in the absence of Shox2. Both neurofilament and lacZ staining of P0 control and Nestin-Cre; Shox2flox/− or Nestin-Cre; Shox2lacZ/flox pup brains demonstrated that the facial motor nucleus was severely reduced in size, with disruptions in neuronal spatial organization in mice lacking Shox2 function (Figure 4a–f, arrows; note that the Shox2lacZ allele is a or severely hypomorphic allele, see “Methods”). While the symmetry between the left and right facial motor nuclei appears to be relatively maintained (Figure 4c–d, arrows), the two lobes that normally comprise the facial motor nucleus are no longer present (Figure 4e–f, arrows). We next investigated whether an increase in apoptosis could account for the changes observed in the facial motor nucleus of Shox2-mutant brains. We found an increase in the number of apoptotic cells present at E12.5 and E14.5 in the facial motor nucleus of Shox2-mutants (Figure 4g–l); however, no significant increase in apoptosis was detected in the E16.5 or P0 facial motor nucleus of Shox2-mutant animals (Figure 4m–r). We observed a ~7.5-fold increase in the number of cleaved active-CASP3 + cells in the E12.5 facial motor nucleus of Nestin-Cre; Shox2flox/− animals as compared to controls (Figure 4i; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0038). We also observed a striking ~17.7-fold increase in the number of cleaved active-CASP3 + cells in the E14.5 facial motor nucleus of Nestin-Cre; Shox2flox/− animals as compared to controls (Figure 4l; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0007). While the slight elevation in apoptosis detected in the E16.5 and P0 facial motor nucleus of Shox2-mutant animals was not significantly different from controls (Figure 4o, r), we did observe a ~3.5-fold increase in the number of cleaved active-CASP3 + cells at P0 when we included the tissue immediately surrounding the facial motor nucleus of Nestin-Cre; Shox2flox/− animals (Figure 4p–q, entire panel including cells within the dashed-circle) in our cell count (Figure 4s; control n = 3, Nestin-Cre; Shox2flox/− n = 3, p = 0.0007). Moreover, when we calculated the area of Shox2lacZ + cells remaining in sagittal sections through the center of the facial motor nucleus of Nestin-Cre; Shox2lacZ/flox animals as compared to controls at E14.5 (Figure 4t) and P0 (Figure 4u), we observed a ~44% decrease in the area of Shox2lacZ + cells in the E14.5 facial motor nucleus (Figure 4v; control n = 3, Nestin-Cre; Shox2lacZ/flox n = 3, p = 0.0027) and a ~53% decrease in the area of Shox2lacZ + cells in the P0 facial motor nucleus (Figure 4w; control n = 3, Nestin-Cre; Shox2lacZ/flox n = 3, p = 0.0011). Therefore, the higher levels of apoptosis are correlated with a decrease in the size of the facial motor nucleus, and taken together, the results demonstrate that apoptosis contributes to the disruptions observed in the facial motor nucleus of Nestin-Cre; Shox2flox/− animals.Figure 4

Bottom Line: Using a Nestin-Cre driver, we show that elimination of Shox2 throughout the brain results in elevated cell death in the facial motor nucleus at embryonic day 12.5 (E12.5) and E14.5, which correlates with impaired axonal projection properties of vMNs.We also observed changes in the spatial expression of the vMN cell fate factors Isl1 and Phox2b, and concomitant defects in Shh and Ptch1 expression in Shox2 mutants.Furthermore, we demonstrate that elimination of Shox2 results in the loss of dorsomedial and ventromedial subnuclei by postnatal day 0 (P0), which may explain the changes in physical activity and impaired feeding/nursing behavior in Shox2 mutants.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., BI286D, Calgary, AB, T2N 1N4, Canada. jmrosin2013@gmail.com.

ABSTRACT

Background: Axons from the visceral motor neurons (vMNs) project from nuclei in the hindbrain to innervate autonomic ganglia and branchial arch-derived muscles. Although much is known about the events that govern specification of somatic motor neurons, the genetic pathways responsible for the development of vMNs are less well characterized. We know that vMNs, like all motor neurons, depend on sonic hedgehog signaling for their generation. Similarly, the paired-like homeobox 2b (Phox2b) gene, which is expressed in both proliferating progenitors and post-mitotic motor neurons, is essential for the development of vMNs. Given that our previous study identified a novel role for the short stature homeobox 2 (Shox2) gene in the hindbrain, and since SHOX2 has been shown to regulate transcription of islet 1 (Isl1), an important regulator of vMN development, we sought to determine whether Shox2 is required for the proper development of the facial motor nucleus.

Results: Using a Nestin-Cre driver, we show that elimination of Shox2 throughout the brain results in elevated cell death in the facial motor nucleus at embryonic day 12.5 (E12.5) and E14.5, which correlates with impaired axonal projection properties of vMNs. We also observed changes in the spatial expression of the vMN cell fate factors Isl1 and Phox2b, and concomitant defects in Shh and Ptch1 expression in Shox2 mutants. Furthermore, we demonstrate that elimination of Shox2 results in the loss of dorsomedial and ventromedial subnuclei by postnatal day 0 (P0), which may explain the changes in physical activity and impaired feeding/nursing behavior in Shox2 mutants.

Conclusions: Combined, our data show that Shox2 is required for development of the facial motor nucleus and its associated facial (VII) nerves, and serves as a new molecular tool to probe the genetic programs of this understudied hindbrain region.

No MeSH data available.


Related in: MedlinePlus