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Developmental Studies Hybridoma Bank mouse anti islet 1 2
Netrin5 keeps MNs cell bodies from migrating out of the CNS.  Immunolabeling of E13.5 embryos showed ectopic MN cell bodies in the ventral roots of  Ntn5 −/−  mutants. Ectopias were not observed in controls  (A) , but cells positive for Islet 1/2  (B)  and HB9  (C)  were observed in mutants, indicative of MNs. While some MNs were positive for nrp2,  (D,E)  ectopic MNs in mutant embyros were not  (D,F) , suggesting that these MNs are a different population from those known to use a semaphorin6A/nrp2 mechanism. Furthermore, there were more ectopias in the rostral half of the embryo than in the caudal (quantified in  G ) which is the inverse of what was observed in  Nrp2  mutant embryos. CNS glia such as GFAP-positive astrocytes did not enter the ventral root  (H,I)  indicating this aspect of the CNS/PNS boundary was not lost. NF, neurofilament. Scale bar is 50 μm. *indicates  P
Mouse Anti Islet 1 2, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Analysis of Expression Pattern and Genetic Deletion of Netrin5 in the Developing Mouse"

Article Title: Analysis of Expression Pattern and Genetic Deletion of Netrin5 in the Developing Mouse

Journal: Frontiers in Molecular Neuroscience

doi: 10.3389/fnmol.2016.00003

Netrin5 keeps MNs cell bodies from migrating out of the CNS.  Immunolabeling of E13.5 embryos showed ectopic MN cell bodies in the ventral roots of  Ntn5 −/−  mutants. Ectopias were not observed in controls  (A) , but cells positive for Islet 1/2  (B)  and HB9  (C)  were observed in mutants, indicative of MNs. While some MNs were positive for nrp2,  (D,E)  ectopic MNs in mutant embyros were not  (D,F) , suggesting that these MNs are a different population from those known to use a semaphorin6A/nrp2 mechanism. Furthermore, there were more ectopias in the rostral half of the embryo than in the caudal (quantified in  G ) which is the inverse of what was observed in  Nrp2  mutant embryos. CNS glia such as GFAP-positive astrocytes did not enter the ventral root  (H,I)  indicating this aspect of the CNS/PNS boundary was not lost. NF, neurofilament. Scale bar is 50 μm. *indicates  P
Figure Legend Snippet: Netrin5 keeps MNs cell bodies from migrating out of the CNS. Immunolabeling of E13.5 embryos showed ectopic MN cell bodies in the ventral roots of Ntn5 −/− mutants. Ectopias were not observed in controls (A) , but cells positive for Islet 1/2 (B) and HB9 (C) were observed in mutants, indicative of MNs. While some MNs were positive for nrp2, (D,E) ectopic MNs in mutant embyros were not (D,F) , suggesting that these MNs are a different population from those known to use a semaphorin6A/nrp2 mechanism. Furthermore, there were more ectopias in the rostral half of the embryo than in the caudal (quantified in G ) which is the inverse of what was observed in Nrp2 mutant embryos. CNS glia such as GFAP-positive astrocytes did not enter the ventral root (H,I) indicating this aspect of the CNS/PNS boundary was not lost. NF, neurofilament. Scale bar is 50 μm. *indicates P

Techniques Used: Immunolabeling, Mutagenesis

DCC is required to prevent ectopic motor neuron migration.  A series of netrin receptor mutant embryos were analyzed at E13.5 for ectopic MNs in the rostral half of the spinal cord. As in controls ( A ,  n  = 3), ectopias were not observed in  Dscam  ( B ,  n  = 3),  Unc5C  ( C ,  n  = 3), or  Neogenin  ( D ,  n  = 2) mutants. There were, however, ectopic MNs in  DCC  mutants ( n  = 4) positive both for Islet 1/2  (E)  and HB9  (F) . Quantified in  (G) . Scale bar in  (F)  is 50 μm. *indicates  P
Figure Legend Snippet: DCC is required to prevent ectopic motor neuron migration. A series of netrin receptor mutant embryos were analyzed at E13.5 for ectopic MNs in the rostral half of the spinal cord. As in controls ( A , n = 3), ectopias were not observed in Dscam ( B , n = 3), Unc5C ( C , n = 3), or Neogenin ( D , n = 2) mutants. There were, however, ectopic MNs in DCC mutants ( n = 4) positive both for Islet 1/2 (E) and HB9 (F) . Quantified in (G) . Scale bar in (F) is 50 μm. *indicates P

Techniques Used: Droplet Countercurrent Chromatography, Migration, Mutagenesis

Related Articles

other:

Article Title: Analysis of Expression Pattern and Genetic Deletion of Netrin5 in the Developing Mouse
Article Snippet: Antibodies Primary antibodies used were as follows: mouse anti-Islet 1/2 (DSHB, clone 39.4D5, 1:500), mouse anti-HB9 (DSHB, clone 81.5C10, 1:500), mouse anti-neurofilament-M (DSHB, clone 2H3, 1:500), rabbit anti-neurofilament (Sigma, 1:500), rabbit anti-Krox20 (Covance, 1:200), rabbit anti-CGRP (Millipore, 1:250), rabbit anti-parvalbumin (Chemicon, 1:500), rabbit anti-GFAP (Sigma, 1:500), rabbit anti-neuropilin-2 (Cell Signaling, 1:250), chicken anti-βGal (Aves, 1:1000).

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    Developmental Studies Hybridoma Bank mouse anti isl1 2
    Trnp1 marks ON type bipolar cells. Immunostaining of developing and adult retinas with Trnp1 ( green ) and cell type-specific markers. ( A – E ) Trnp1 costaining with Otx2 ( red ) and Pax6 ( gray ) at multiple ages. Otx2 is cropped and Pax6 shown only in the insets for clarity. At P0 ( A ) and P5 ( B ), no Trnp1 immunostaining is detected in the retina. ( C ) Starting at P7, Trnp1 nuclear staining is seen in the INL, where it overlaps completely with Otx2 ( arrows , insets ). The same pattern of Trnp1 expression is seen at P10 ( D ) and in adult ( E ) sections. Pax6+ amacrine cells in the ONL ( arrowheads , insets ) do not coexpress Trnp1 at any age. ( F – K ) Adult sections stained with Trnp1 and bipolar subtype specific markers ( red / gray ). ( F ) Cells that are Trnp1+ coexpress <t>Isl1/2</t> ( red , arrows , insets ), which marks ON type bipolar cells in the retina. Starburst amacrines labeled by Isl1/2 ( arrowheads ) do not express Trnp1. ( G – G'' ) A section showing Trnp1, Scgn ( gray ) and PKCα ( red ) costaining. A subset of Trnp1+ cells coexpresses Scgn ( arrowheads , insets ) or PKCα ( arrows , insets ). Nearly all of the PKCα+ rod bipolar cells express Trnp1 (G''), but only a fraction of Scgn+ cone bipolars are Trnp1+ ( G' ). ( H ) Type 2 cone OFF bipolar cells marked by Bhlhb5 staining ( arrowheads , insets ) do not coexpress Trnp1. Bhlhb5+ amacrine cells are marked with an “a”. ( I ) Calsenilin-positive type 4 cone OFF bipolar cells ( arrowheads , insets ) do not coexpress Trnp1. Scale bars : ( A – E , G – H ) 25 μm for panels and 10 μm for insets; ( F ) 100 μm and 10 μm for insets; ( I ) 50 μm and 10 μm for the insets. ( J ) Quantification of Trnp1 staining in the adult wild-type retina. The left panel shows the fraction of Trnp1+ cells that coexpress a cell-type specific marker. The right panel shows what percentage of a given population of cells expresses Trnp1. Error bars represent SD.
    Mouse Anti Isl1 2, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 89/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Developmental Studies Hybridoma Bank mouse anti isl1
    Hb9::Cre-derived INs do not overlap with the Shox2 non-V2a population. ( A ) Co-expression of YFP (green) and <t>Isl1</t> antibody (red) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Motor neurons are also labeled by Isl1 antibody (blue box). Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Isl1 (red) and Hb9::Cre-derived INs (green). Scale bars: 100 μm and 50 μm. ( B ) Co-expression of YFP (green), Shox2 antibody (red) and/or Chx10 antibody (blue) in the Hb9 :: Cre;Rosa26-YFP mouse ventral spinal cord at E11.5. Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Hb9::Cre-derived INs (green) and Shox2 + Chx10 − (red), Shox2 − Chx10 + (blue) or Shox2 + Chx10 + (pink). Scale bars: 100 μm and 50 μm. ( C ) Quantification of overlap in (A) and (B). Bar graph showing percent of overlap between Hb9::Cre-derived INs (YFP + ) and Shox2 V2a (Shox2 + Chx10 + , 4% ± 1%), Shox2 OFF V2a (Shox2 − Chx10 + , 2% ± 0.1%), Shox2 non-V2a (Shox2 + Chx10 − , 1.3% ± 0.2%), and Isl1 (Isl1 + , 6% ± 0.2%) INs. Error bars represent ± SEM. ( D ) Percent of the Shox2 non-V2a IN population (Shox2 + Chx10 − ) that overlaps with Hb9::Cre-derived INs (YFP + ) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Shox2 non-V2a INs rarely co-express YFP (Shox2 + YFP + , darker grey) (12% ± 2%). Error bars represent ± SEM.
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    Developmental Studies Hybridoma Bank anti islet 1 2
    Delayed differentiation of postnatal cochlear ganglion in Igf-1 −/− mice. Immunohistochemical analysis of paraffin sections of the cochlear ganglion at midmodiolar levels using nestin ( A–D ), <t>Islet-1/2</t> ( E–H ), synaptophysin ( I–L ), myelin P 0 ( M–P ), and GFAP ( Q–T ) antibodies. Left panels ( A , E , I , M, Q ) correspond to P5 Igf-1 +/+ samples, middle-left panels ( B, F, J, N, R ) to P5 Igf-1 −/− , middle-right panels ( C, G, K, O, S ) are from P20 Igf-1 +/+ , and right panels ( D, H, L, P , T ) from P20 Igf-1 −/− mice. E–H correspond to basal turns of the cochlear ganglion, and the remaining sections in the figure are from apical turns. Scale bars: A–L , 40 μm; M–T, 30 μm.
    Anti Islet 1 2, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 88/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Trnp1 marks ON type bipolar cells. Immunostaining of developing and adult retinas with Trnp1 ( green ) and cell type-specific markers. ( A – E ) Trnp1 costaining with Otx2 ( red ) and Pax6 ( gray ) at multiple ages. Otx2 is cropped and Pax6 shown only in the insets for clarity. At P0 ( A ) and P5 ( B ), no Trnp1 immunostaining is detected in the retina. ( C ) Starting at P7, Trnp1 nuclear staining is seen in the INL, where it overlaps completely with Otx2 ( arrows , insets ). The same pattern of Trnp1 expression is seen at P10 ( D ) and in adult ( E ) sections. Pax6+ amacrine cells in the ONL ( arrowheads , insets ) do not coexpress Trnp1 at any age. ( F – K ) Adult sections stained with Trnp1 and bipolar subtype specific markers ( red / gray ). ( F ) Cells that are Trnp1+ coexpress Isl1/2 ( red , arrows , insets ), which marks ON type bipolar cells in the retina. Starburst amacrines labeled by Isl1/2 ( arrowheads ) do not express Trnp1. ( G – G'' ) A section showing Trnp1, Scgn ( gray ) and PKCα ( red ) costaining. A subset of Trnp1+ cells coexpresses Scgn ( arrowheads , insets ) or PKCα ( arrows , insets ). Nearly all of the PKCα+ rod bipolar cells express Trnp1 (G''), but only a fraction of Scgn+ cone bipolars are Trnp1+ ( G' ). ( H ) Type 2 cone OFF bipolar cells marked by Bhlhb5 staining ( arrowheads , insets ) do not coexpress Trnp1. Bhlhb5+ amacrine cells are marked with an “a”. ( I ) Calsenilin-positive type 4 cone OFF bipolar cells ( arrowheads , insets ) do not coexpress Trnp1. Scale bars : ( A – E , G – H ) 25 μm for panels and 10 μm for insets; ( F ) 100 μm and 10 μm for insets; ( I ) 50 μm and 10 μm for the insets. ( J ) Quantification of Trnp1 staining in the adult wild-type retina. The left panel shows the fraction of Trnp1+ cells that coexpress a cell-type specific marker. The right panel shows what percentage of a given population of cells expresses Trnp1. Error bars represent SD.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Gsg1, Trnp1, and Tmem215 Mark Subpopulations of Bipolar Interneurons in the Mouse Retina

    doi: 10.1167/iovs.16-19767

    Figure Lengend Snippet: Trnp1 marks ON type bipolar cells. Immunostaining of developing and adult retinas with Trnp1 ( green ) and cell type-specific markers. ( A – E ) Trnp1 costaining with Otx2 ( red ) and Pax6 ( gray ) at multiple ages. Otx2 is cropped and Pax6 shown only in the insets for clarity. At P0 ( A ) and P5 ( B ), no Trnp1 immunostaining is detected in the retina. ( C ) Starting at P7, Trnp1 nuclear staining is seen in the INL, where it overlaps completely with Otx2 ( arrows , insets ). The same pattern of Trnp1 expression is seen at P10 ( D ) and in adult ( E ) sections. Pax6+ amacrine cells in the ONL ( arrowheads , insets ) do not coexpress Trnp1 at any age. ( F – K ) Adult sections stained with Trnp1 and bipolar subtype specific markers ( red / gray ). ( F ) Cells that are Trnp1+ coexpress Isl1/2 ( red , arrows , insets ), which marks ON type bipolar cells in the retina. Starburst amacrines labeled by Isl1/2 ( arrowheads ) do not express Trnp1. ( G – G'' ) A section showing Trnp1, Scgn ( gray ) and PKCα ( red ) costaining. A subset of Trnp1+ cells coexpresses Scgn ( arrowheads , insets ) or PKCα ( arrows , insets ). Nearly all of the PKCα+ rod bipolar cells express Trnp1 (G''), but only a fraction of Scgn+ cone bipolars are Trnp1+ ( G' ). ( H ) Type 2 cone OFF bipolar cells marked by Bhlhb5 staining ( arrowheads , insets ) do not coexpress Trnp1. Bhlhb5+ amacrine cells are marked with an “a”. ( I ) Calsenilin-positive type 4 cone OFF bipolar cells ( arrowheads , insets ) do not coexpress Trnp1. Scale bars : ( A – E , G – H ) 25 μm for panels and 10 μm for insets; ( F ) 100 μm and 10 μm for insets; ( I ) 50 μm and 10 μm for the insets. ( J ) Quantification of Trnp1 staining in the adult wild-type retina. The left panel shows the fraction of Trnp1+ cells that coexpress a cell-type specific marker. The right panel shows what percentage of a given population of cells expresses Trnp1. Error bars represent SD.

    Article Snippet: Primary antibodies used were: mouse anti-Ap2α (1:250, clone 5E4; Developmental Studies Hybridoma Bank, Iowa City, IA, USA); chicken anti–β-galactosidase (β-gal; 1:2000, AB9361; Abcam, Cambridge, MA, USA); goat anti-Bhlhb5 (1:1000, sc-6045; Santa Cruz Biotechnology, Inc., Dallas, TX, USA); mouse anti-Cabp5 (1:10, a gift from F. Haeseleer, University of Washington) ; mouse anti-Calretinin (1:750) (MAB1568, Milipore, Billerica, MA, USA); mouse anti-Calsenilin (1:2000, 05-756; Milipore); rabbit anti-GAD65/67 (1:500, AB1511; Milipore); goat anti-GlyT1 (1:2000, AB1770; Milipore); rabbit anti-HCN4 (1:500, APC-052; Alomone Labs Ltd., Jerusalem, Israel); mouse anti-Isl1/2 (1:250, clone 39.4D5; Developmental Studies Hybridoma Bank); goat anti-Otx2 (1:200, BAF1979; R & D Systems, Minneapolis, MN, USA); rabbit anti-Pax6 (1:500, 901301; BioLegend, Inc., San Diego, CA, USA); mouse anti-PKARIIβ (1:3000, 610625; BD Biosciences, San Jose, CA, USA); mouse anti-PKCα (1:250, P5704; Sigma-Aldrich Corp., St. Louis, MO, USA); rabbit anti-Scgn (1:5000, RD181120100; Biovendor LLC, Ashville, NC, USA); goat anti-Sox2 (1:100, sc17320; Santa Cruz Biotechnology); guinea pig anti-Trnp1 (1:200, a gift from M. Götz, Helmholtz Zentrum Muenchen) ; and rabbit anti-Vsx1 (1:250, a gift from E. Levine, Vanderbilt University).

    Techniques: Immunostaining, Staining, Expressing, Labeling, Marker

    Tmem215 marks subsets of bipolar and amacrine cells. Adult Tmem215-LacZ heterozygous mice stained for β-gal ( green ) and cell-type specific markers ( red / gray ). ( A – A' ) Section stained with Scgn ( gray ) and PKCα ( red ). A large fraction of β-gal+ cells coexpress Scgn ( arrows , insets ), but none overlap with PKCα ( arrowheads , insets ). ( B ) Costaining with Scgn ( gray ) and Isl1/2 ( red ) to mark ON bipolar cells. A subset of β-gal+ cells coexpress Isl1/2 ( arrows , blue insets ). Other β-gal+ cells coexpress only Scgn ( arrowheads ), marking them as cone OFF bipolars. Thus, Tmem215-LacZ marks both ON and OFF cone bipolar cells. ( C – C' ) Costaining with Isl1/2 ( gray ) and Vsx1 ( red ), which mark types 1, 2, and 7 cone bipolars. A subset of β-gal+ cells coexpress Vsx1 and Isl1/2 ( arrows , insets ), marking them as type 7 cone ON bipolars. However, not all type 7 cone bipolars were β-gal+ ( magenta arrowheads , insets ). Some β-gal+ cells expressed Isl1/2, but not Vsx1 ( arrowheads , insets ). Of the β-gal+ cells that did not express Isl1/2, none coexpressed Vsx1 ( asterisks ). This argues that types 1 and 2 cone bipolars are not Tmem215+. Isl1/2+ amacrine cells do not coexpress β-gal. ( D ) A subset of β-gal+ cells coexpress Cabp5 ( red , arrows , insets ), which marks types 3 and 5 cone bipolars. ( E ) β-gal costaining with HCN4 to mark type 3a cone OFF bipolars. Most HCN4+ bipolar cells coexpress β-gal ( arrows , insets ), though some HCN4+ cells in the inner INL lack β-gal staining ( arrowheads ). ( F ) β-gal expression ( arrowheads , insets ) does not overlap with PKARIIβ ( red ), a marker of type 3b cone bipolars. ( G ) Type 2 cone OFF bipolars marked with Bhlhb5 did not express β-gal ( arrowheads , insets ). We did not see β-gal overlap with the type 4 cone OFF bipolar marker Csen (data not shown). ( H – H' ) Retinas stained with the amacrine markers GlyT1 ( red , glycinergic) and GAD65/67 ( gray , GABAergic). Roughly equal fractions coexpress GlyT1 ( arrows , insets ) and GAD65/67 ( arrowheads , insets ). There are no β-gal+ displaced amacrine cells seen. ( I ) A subset of the β-gal+ amacrine cells ( arrowheads , insets ) coexpress Ap2α ( red ) ( arrows , insets ). Scale bars : 50 μm for panels and 10 μm for insets. ( J ) Quantification of β-gal+ cells. The left panel shows the percentage of β-gal+ cells that coexpress a cell type–specific marker. There are approximately 9 β-gal+ bipolar cells (Otx2+) for every amacrine cell (Pax6+). The right panel shows the fraction of a cell type–specific marker population that coexpresses β-gal+. Error bars show SD.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Gsg1, Trnp1, and Tmem215 Mark Subpopulations of Bipolar Interneurons in the Mouse Retina

    doi: 10.1167/iovs.16-19767

    Figure Lengend Snippet: Tmem215 marks subsets of bipolar and amacrine cells. Adult Tmem215-LacZ heterozygous mice stained for β-gal ( green ) and cell-type specific markers ( red / gray ). ( A – A' ) Section stained with Scgn ( gray ) and PKCα ( red ). A large fraction of β-gal+ cells coexpress Scgn ( arrows , insets ), but none overlap with PKCα ( arrowheads , insets ). ( B ) Costaining with Scgn ( gray ) and Isl1/2 ( red ) to mark ON bipolar cells. A subset of β-gal+ cells coexpress Isl1/2 ( arrows , blue insets ). Other β-gal+ cells coexpress only Scgn ( arrowheads ), marking them as cone OFF bipolars. Thus, Tmem215-LacZ marks both ON and OFF cone bipolar cells. ( C – C' ) Costaining with Isl1/2 ( gray ) and Vsx1 ( red ), which mark types 1, 2, and 7 cone bipolars. A subset of β-gal+ cells coexpress Vsx1 and Isl1/2 ( arrows , insets ), marking them as type 7 cone ON bipolars. However, not all type 7 cone bipolars were β-gal+ ( magenta arrowheads , insets ). Some β-gal+ cells expressed Isl1/2, but not Vsx1 ( arrowheads , insets ). Of the β-gal+ cells that did not express Isl1/2, none coexpressed Vsx1 ( asterisks ). This argues that types 1 and 2 cone bipolars are not Tmem215+. Isl1/2+ amacrine cells do not coexpress β-gal. ( D ) A subset of β-gal+ cells coexpress Cabp5 ( red , arrows , insets ), which marks types 3 and 5 cone bipolars. ( E ) β-gal costaining with HCN4 to mark type 3a cone OFF bipolars. Most HCN4+ bipolar cells coexpress β-gal ( arrows , insets ), though some HCN4+ cells in the inner INL lack β-gal staining ( arrowheads ). ( F ) β-gal expression ( arrowheads , insets ) does not overlap with PKARIIβ ( red ), a marker of type 3b cone bipolars. ( G ) Type 2 cone OFF bipolars marked with Bhlhb5 did not express β-gal ( arrowheads , insets ). We did not see β-gal overlap with the type 4 cone OFF bipolar marker Csen (data not shown). ( H – H' ) Retinas stained with the amacrine markers GlyT1 ( red , glycinergic) and GAD65/67 ( gray , GABAergic). Roughly equal fractions coexpress GlyT1 ( arrows , insets ) and GAD65/67 ( arrowheads , insets ). There are no β-gal+ displaced amacrine cells seen. ( I ) A subset of the β-gal+ amacrine cells ( arrowheads , insets ) coexpress Ap2α ( red ) ( arrows , insets ). Scale bars : 50 μm for panels and 10 μm for insets. ( J ) Quantification of β-gal+ cells. The left panel shows the percentage of β-gal+ cells that coexpress a cell type–specific marker. There are approximately 9 β-gal+ bipolar cells (Otx2+) for every amacrine cell (Pax6+). The right panel shows the fraction of a cell type–specific marker population that coexpresses β-gal+. Error bars show SD.

    Article Snippet: Primary antibodies used were: mouse anti-Ap2α (1:250, clone 5E4; Developmental Studies Hybridoma Bank, Iowa City, IA, USA); chicken anti–β-galactosidase (β-gal; 1:2000, AB9361; Abcam, Cambridge, MA, USA); goat anti-Bhlhb5 (1:1000, sc-6045; Santa Cruz Biotechnology, Inc., Dallas, TX, USA); mouse anti-Cabp5 (1:10, a gift from F. Haeseleer, University of Washington) ; mouse anti-Calretinin (1:750) (MAB1568, Milipore, Billerica, MA, USA); mouse anti-Calsenilin (1:2000, 05-756; Milipore); rabbit anti-GAD65/67 (1:500, AB1511; Milipore); goat anti-GlyT1 (1:2000, AB1770; Milipore); rabbit anti-HCN4 (1:500, APC-052; Alomone Labs Ltd., Jerusalem, Israel); mouse anti-Isl1/2 (1:250, clone 39.4D5; Developmental Studies Hybridoma Bank); goat anti-Otx2 (1:200, BAF1979; R & D Systems, Minneapolis, MN, USA); rabbit anti-Pax6 (1:500, 901301; BioLegend, Inc., San Diego, CA, USA); mouse anti-PKARIIβ (1:3000, 610625; BD Biosciences, San Jose, CA, USA); mouse anti-PKCα (1:250, P5704; Sigma-Aldrich Corp., St. Louis, MO, USA); rabbit anti-Scgn (1:5000, RD181120100; Biovendor LLC, Ashville, NC, USA); goat anti-Sox2 (1:100, sc17320; Santa Cruz Biotechnology); guinea pig anti-Trnp1 (1:200, a gift from M. Götz, Helmholtz Zentrum Muenchen) ; and rabbit anti-Vsx1 (1:250, a gift from E. Levine, Vanderbilt University).

    Techniques: Mouse Assay, Staining, Expressing, Marker

    mSix1-8-NLSCre induces sensory neuron-specific recombination in mouse embryos. (A-I) Immunofluorescence analysis of Cre-mediated recombination in mSix1-8-NLSCre/R26R-LacZ double transgenic embryos. Distribution of ß-Gal was examined at E10.5 (A-D, H), E11.5 (E) and E12.5 (F, G). At E10.5, ß-Gal (Aa) co-localized with a neuron marker ISL1/2 (Aa') in the trigeminal ganglion (yellow signals in Aa''), geniculate-vestibuloacoustic ganglion complex (Ba, Ba', Ba''), petrosal ganglion (Ca, Ca', Ca'') and nodose ganglion (Da, Da', Da'') in transverse sections through the cervical area. In contrast, the same sections stained for a glial marker SOX10 showed no overlap of ß-Gal (green)-positive cells with SOX10 (red)-positive cells in all cranial sensory ganglia (Ab, Bb, Cb, Db). At E11.5, ß-Gal (Ea) also co-localized with ISL1/2 (Ea') in the DRG (yellow signals in Ea'') in a transverse section through the trunk region but not with SOX10 on the same section (Eb). In the frontal sections through the OE at E12.5 (F, G), ß-Gal (green)-positive cells were detected not only in the OE (F, G) but also in the vomeronasal organ (G) and in the surrounding mesenchyme along the TUBB3 (red)-positive axons of the olfactory and vomeronasal sensory neurons (white arrowheads). Many ß-Gal-positive cells were also found in the

    Journal: PLoS ONE

    Article Title: Activation of Six1 Expression in Vertebrate Sensory Neurons

    doi: 10.1371/journal.pone.0136666

    Figure Lengend Snippet: mSix1-8-NLSCre induces sensory neuron-specific recombination in mouse embryos. (A-I) Immunofluorescence analysis of Cre-mediated recombination in mSix1-8-NLSCre/R26R-LacZ double transgenic embryos. Distribution of ß-Gal was examined at E10.5 (A-D, H), E11.5 (E) and E12.5 (F, G). At E10.5, ß-Gal (Aa) co-localized with a neuron marker ISL1/2 (Aa') in the trigeminal ganglion (yellow signals in Aa''), geniculate-vestibuloacoustic ganglion complex (Ba, Ba', Ba''), petrosal ganglion (Ca, Ca', Ca'') and nodose ganglion (Da, Da', Da'') in transverse sections through the cervical area. In contrast, the same sections stained for a glial marker SOX10 showed no overlap of ß-Gal (green)-positive cells with SOX10 (red)-positive cells in all cranial sensory ganglia (Ab, Bb, Cb, Db). At E11.5, ß-Gal (Ea) also co-localized with ISL1/2 (Ea') in the DRG (yellow signals in Ea'') in a transverse section through the trunk region but not with SOX10 on the same section (Eb). In the frontal sections through the OE at E12.5 (F, G), ß-Gal (green)-positive cells were detected not only in the OE (F, G) but also in the vomeronasal organ (G) and in the surrounding mesenchyme along the TUBB3 (red)-positive axons of the olfactory and vomeronasal sensory neurons (white arrowheads). Many ß-Gal-positive cells were also found in the "migratory mass (white square bracket)" comprising placode-derived migratory cells and axons of olfactory sensory neurons located ventral to the forebrain (F). (H) At E10.5, ß-Gal (green)-positive cells were found in the OE (demarcated by white dotted line) and in an aggregate of TUBB3-positive cells (white arrowheads) located next to the OE. (I) Immunofluorescence analysis of Six1-8 enhancer activity in chick. Frontal section through the olfactory pit of a representative chick embryo at 48 h.p.e. EGFP (green) derived from pT2A-BB-mSix1-8-EGFP was detected in the OE and in an aggregate of TUBB3 (red)-positive cells (yellow arrow) located subjacent to the OE, a likely avian homolog of the rodent migratory mass. DAPI was used for nuclear staining (blue, Aa'', Ab, Ba'', Bb, Ca'', Cb, Da'', Db, Ea'', Eb, F-I). In all panels, dorsal is to the top and midline is to the left (A-E , H) or right (F, G, P). drg: dorsal root ganglia, fb: forebrain, mm: migratory mass, oe: olfactory epithelium, ov: otic vesicle, vno: vomeronasal organ, V: trigeminal ganglia, VII: geniculate ganglia, VIII: vestibuloacoustic ganglion, IX: petrosal ganglion, X: nodose ganglion. Scale bars: 0.1 mm (A-I).

    Article Snippet: The following primary antibodies were used: rabbit anti-ß-Gal (dilution, 1:5000, Covance, Berkeley, CA), mouse anti-ISL1/2 (dilution, 1:150, mixture of hybridoma supernatants, 39.4D5 and 40.2D6, Developmental Studies Hybridoma Bank), rat anti-SIX1 [ ] (dilution, 1:2000), guinea pig anti-SOX10 [ ] (dilution, 1:20000), and mouse anti-TUBB3 (tubulin, beta 3 class III, clone TuJ1, dilution, 1:3000, Covance, Berkeley, CA) antibodies.

    Techniques: Immunofluorescence, Transgenic Assay, Marker, Staining, Derivative Assay, Activity Assay

    Hb9::Cre-derived INs do not overlap with the Shox2 non-V2a population. ( A ) Co-expression of YFP (green) and Isl1 antibody (red) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Motor neurons are also labeled by Isl1 antibody (blue box). Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Isl1 (red) and Hb9::Cre-derived INs (green). Scale bars: 100 μm and 50 μm. ( B ) Co-expression of YFP (green), Shox2 antibody (red) and/or Chx10 antibody (blue) in the Hb9 :: Cre;Rosa26-YFP mouse ventral spinal cord at E11.5. Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Hb9::Cre-derived INs (green) and Shox2 + Chx10 − (red), Shox2 − Chx10 + (blue) or Shox2 + Chx10 + (pink). Scale bars: 100 μm and 50 μm. ( C ) Quantification of overlap in (A) and (B). Bar graph showing percent of overlap between Hb9::Cre-derived INs (YFP + ) and Shox2 V2a (Shox2 + Chx10 + , 4% ± 1%), Shox2 OFF V2a (Shox2 − Chx10 + , 2% ± 0.1%), Shox2 non-V2a (Shox2 + Chx10 − , 1.3% ± 0.2%), and Isl1 (Isl1 + , 6% ± 0.2%) INs. Error bars represent ± SEM. ( D ) Percent of the Shox2 non-V2a IN population (Shox2 + Chx10 − ) that overlaps with Hb9::Cre-derived INs (YFP + ) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Shox2 non-V2a INs rarely co-express YFP (Shox2 + YFP + , darker grey) (12% ± 2%). Error bars represent ± SEM.

    Journal: Scientific Reports

    Article Title: Spinal Hb9::Cre-derived excitatory interneurons contribute to rhythm generation in the mouse

    doi: 10.1038/srep41369

    Figure Lengend Snippet: Hb9::Cre-derived INs do not overlap with the Shox2 non-V2a population. ( A ) Co-expression of YFP (green) and Isl1 antibody (red) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Motor neurons are also labeled by Isl1 antibody (blue box). Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Isl1 (red) and Hb9::Cre-derived INs (green). Scale bars: 100 μm and 50 μm. ( B ) Co-expression of YFP (green), Shox2 antibody (red) and/or Chx10 antibody (blue) in the Hb9 :: Cre;Rosa26-YFP mouse ventral spinal cord at E11.5. Rightmost pictures are magnifications of the white boxed area. Arrowheads indicate overlap between Hb9::Cre-derived INs (green) and Shox2 + Chx10 − (red), Shox2 − Chx10 + (blue) or Shox2 + Chx10 + (pink). Scale bars: 100 μm and 50 μm. ( C ) Quantification of overlap in (A) and (B). Bar graph showing percent of overlap between Hb9::Cre-derived INs (YFP + ) and Shox2 V2a (Shox2 + Chx10 + , 4% ± 1%), Shox2 OFF V2a (Shox2 − Chx10 + , 2% ± 0.1%), Shox2 non-V2a (Shox2 + Chx10 − , 1.3% ± 0.2%), and Isl1 (Isl1 + , 6% ± 0.2%) INs. Error bars represent ± SEM. ( D ) Percent of the Shox2 non-V2a IN population (Shox2 + Chx10 − ) that overlaps with Hb9::Cre-derived INs (YFP + ) in the Hb9 :: Cre;Rosa26-YFP mouse spinal cord at E11.5. Shox2 non-V2a INs rarely co-express YFP (Shox2 + YFP + , darker grey) (12% ± 2%). Error bars represent ± SEM.

    Article Snippet: Sections were incubated for 24 hours with one or several of the following primary antibodies: rabbit anti-Shox2 #860 (1:32,000, generated against the peptide CKTTSKNSSIADLR), sheep anti-Chx10 (1:400, Chemicon), mouse anti-Isl1 (40.2D6 and 39.4D5) (1:250, DSHB), rabbit anti-Hb9 (1:16000, DSHB).

    Techniques: Derivative Assay, Expressing, Labeling

    Delayed differentiation of postnatal cochlear ganglion in Igf-1 −/− mice. Immunohistochemical analysis of paraffin sections of the cochlear ganglion at midmodiolar levels using nestin ( A–D ), Islet-1/2 ( E–H ), synaptophysin ( I–L ), myelin P 0 ( M–P ), and GFAP ( Q–T ) antibodies. Left panels ( A , E , I , M, Q ) correspond to P5 Igf-1 +/+ samples, middle-left panels ( B, F, J, N, R ) to P5 Igf-1 −/− , middle-right panels ( C, G, K, O, S ) are from P20 Igf-1 +/+ , and right panels ( D, H, L, P , T ) from P20 Igf-1 −/− mice. E–H correspond to basal turns of the cochlear ganglion, and the remaining sections in the figure are from apical turns. Scale bars: A–L , 40 μm; M–T, 30 μm.

    Journal: The Journal of Neuroscience

    Article Title: Delayed Inner Ear Maturation and Neuronal Loss in PostnatalIgf-1-Deficient Mice

    doi: 10.1523/JNEUROSCI.21-19-07630.2001

    Figure Lengend Snippet: Delayed differentiation of postnatal cochlear ganglion in Igf-1 −/− mice. Immunohistochemical analysis of paraffin sections of the cochlear ganglion at midmodiolar levels using nestin ( A–D ), Islet-1/2 ( E–H ), synaptophysin ( I–L ), myelin P 0 ( M–P ), and GFAP ( Q–T ) antibodies. Left panels ( A , E , I , M, Q ) correspond to P5 Igf-1 +/+ samples, middle-left panels ( B, F, J, N, R ) to P5 Igf-1 −/− , middle-right panels ( C, G, K, O, S ) are from P20 Igf-1 +/+ , and right panels ( D, H, L, P , T ) from P20 Igf-1 −/− mice. E–H correspond to basal turns of the cochlear ganglion, and the remaining sections in the figure are from apical turns. Scale bars: A–L , 40 μm; M–T, 30 μm.

    Article Snippet: Sources, dilution, and cell specificity of the antibodies used in this study were: anti-proliferative cell nuclear antigen (PCNA) mouse monoclonal (Concepta, Barcelona, Spain) (1:500); anti-caspase-3 activated mouse polyclonal ( ) (1:100); anti-Islet 1/2, mouse monoclonal (Developmental Studies Hybridoma Bank) (1:200); anti-Nestin 128, rabbit polyclonal ( ) (1:500); anti-Neurofilament 200 kDa, mouse monoclonal (Diagnostic, Mannheim, Germany) (1:50); anti-synaptophysin, rabbit polyclonal (Dako, Copenhagen, Denmark) (1:100); anti-GFAP, rabbit polyclonal (Dako) (1:100); anti-Myelin P0 , mouse monoclonal ( ) (1:500); and anti-vimentin VIM3B4 mouse monoclonal ( ) (Profer Immuno-Diagnostika, Heidelberg, Germany) (1:100).

    Techniques: Mouse Assay, Immunohistochemistry