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mouse anti ena (Developmental Studies Hybridoma Bank)

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Developmental Studies Hybridoma Bank mouse anti ena

(A–E) SGPs were detected by in situ hybridization with a 412 retrotransposon RNA probe (blue). PGCs were labeled with anti-Vasa (Vas) antibody (brown). The brown signal in a segmental pattern is β-galastosidase from the balancer chromosome. In wild type, individual SGP clusters align with PGCs at stage 13 (A) and undergo coalescence to form tightly associated embryonic gonads at stage 14 to 16 (B). In <t>ena</t> C14-06 mutants, individual SGP clusters fail or delay to adhere at stage 13, remaining instead in three clusters (arrows in C). Subsequently, mutant gonads fail to complete coalescence resulting in elongated (bracket in D) or split gonads (arrows in E). (F–H) Ena protein detected with <t>anti-Ena</t> antibody. Ena protein is expressed ubiquitously in the wild type (F). Ena protein was not detected in ena C14-06 mutants either by tissue-immuno fluorescence (G) or Western blotting (H). Scale bar in (A) represents 50 µm.

Mouse Anti Ena, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+anti-enabled+5g2/5G2+anti-enabled/pmc03530444-185-13-19
Average 94 stars, based on 65 article reviews

mouse anti ena - by Bioz Stars, 2026-09

94/100 stars

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1) Product Images from "The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis"

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0052649

Figure Legend Snippet: (A–E) SGPs were detected by in situ hybridization with a 412 retrotransposon RNA probe (blue). PGCs were labeled with anti-Vasa (Vas) antibody (brown). The brown signal in a segmental pattern is β-galastosidase from the balancer chromosome. In wild type, individual SGP clusters align with PGCs at stage 13 (A) and undergo coalescence to form tightly associated embryonic gonads at stage 14 to 16 (B). In ena C14-06 mutants, individual SGP clusters fail or delay to adhere at stage 13, remaining instead in three clusters (arrows in C). Subsequently, mutant gonads fail to complete coalescence resulting in elongated (bracket in D) or split gonads (arrows in E). (F–H) Ena protein detected with anti-Ena antibody. Ena protein is expressed ubiquitously in the wild type (F). Ena protein was not detected in ena C14-06 mutants either by tissue-immuno fluorescence (G) or Western blotting (H). Scale bar in (A) represents 50 µm.

Techniques Used: In Situ Hybridization, Labeling, Mutagenesis, Fluorescence, Western Blot

(A–C) Stage-12 embryo stained with the anti-Ena antibody (magenta in A–B, white in C) and anti-Vas antibody to detect PGCs (green). The posterior half of the embryo is shown in (A), migrating PGCs are magnified in (B, C) (asterisks). Ena protein is found at the cell membranes (A) but not in migrating PGCs (B, C). (D–L) Ena expression during gonad coalescence. Wild-type embryos were stained with anti-Ena (magenta), anti-Zfh-1 antibodies, which mark the nuclei of the fat body and SGPs (green), and anti-Vas (PGCs in blue). Ena levels in the SGPs were indistinguishable from those in the surrounding tissues (D, high magnification in E, F). Ena expression in the SGPs was more pronounced in the mature gonad (G, J, high magnification in H–I and K–L). The scale bars in (A and D), (B), and (E) represent 50 µm, 10 µm, and 20 µm, respectively.

Figure Legend Snippet: (A–C) Stage-12 embryo stained with the anti-Ena antibody (magenta in A–B, white in C) and anti-Vas antibody to detect PGCs (green). The posterior half of the embryo is shown in (A), migrating PGCs are magnified in (B, C) (asterisks). Ena protein is found at the cell membranes (A) but not in migrating PGCs (B, C). (D–L) Ena expression during gonad coalescence. Wild-type embryos were stained with anti-Ena (magenta), anti-Zfh-1 antibodies, which mark the nuclei of the fat body and SGPs (green), and anti-Vas (PGCs in blue). Ena levels in the SGPs were indistinguishable from those in the surrounding tissues (D, high magnification in E, F). Ena expression in the SGPs was more pronounced in the mature gonad (G, J, high magnification in H–I and K–L). The scale bars in (A and D), (B), and (E) represent 50 µm, 10 µm, and 20 µm, respectively.

Techniques Used: Staining, Expressing

(A–F) Rescue experiment of ena mutants. The coalescence phenotype at stages 15–16 was categorized into severe (green), intermediate (red), and normal classes (blue) as illustrated in (A), and number of gonads scored is indicated above the graph (B). Germline expression of Ena by nanos (nos) -Gal4 did not show any rescue activity (B) albeit the Ena protein derived from the transgene was detected in PGCs (blue in E and F). Ena expression in the mesoderm by 24B-Gal4 partially rescued the compaction phenotype in the mutants (B). (G–J) ena function was tested in a maternal oskar mutant background lacking PGCs. The 412 retrotransposon probe was used to label SGPs (blue). In maternal oskar mutants, SGPs were specified normally and compacted into spherical ‘gonads’ (G and H). In ena (zygotic), oskar (maternal) double mutants, SGP clusters failed to adhere at stage 13 (I), resulting in elongated gonads similar to those in zygotic ena mutants (J). (K–L) The stage-15 embryos were stained with anti-Serpent and anti-Vas antibodies to detect the fat body (magenta, bracket) and PGCs (green). The fat body appears unaffected by the ena mutation. Scale bars in (A) and (D) represent 50 µm.

Figure Legend Snippet: (A–F) Rescue experiment of ena mutants. The coalescence phenotype at stages 15–16 was categorized into severe (green), intermediate (red), and normal classes (blue) as illustrated in (A), and number of gonads scored is indicated above the graph (B). Germline expression of Ena by nanos (nos) -Gal4 did not show any rescue activity (B) albeit the Ena protein derived from the transgene was detected in PGCs (blue in E and F). Ena expression in the mesoderm by 24B-Gal4 partially rescued the compaction phenotype in the mutants (B). (G–J) ena function was tested in a maternal oskar mutant background lacking PGCs. The 412 retrotransposon probe was used to label SGPs (blue). In maternal oskar mutants, SGPs were specified normally and compacted into spherical ‘gonads’ (G and H). In ena (zygotic), oskar (maternal) double mutants, SGP clusters failed to adhere at stage 13 (I), resulting in elongated gonads similar to those in zygotic ena mutants (J). (K–L) The stage-15 embryos were stained with anti-Serpent and anti-Vas antibodies to detect the fat body (magenta, bracket) and PGCs (green). The fat body appears unaffected by the ena mutation. Scale bars in (A) and (D) represent 50 µm.

Techniques Used: Expressing, Activity Assay, Derivative Assay, Mutagenesis, Staining

(A–F) Wild-type and ena mutant embryos with the P six4 -egfp::moesin transgene were double stained with anti-GFP (green) and anti-Vas (magenta) antibodies. Labeled gonads at stages 15–16 were scanned and rendered into 3D images. Z projection (A, C, E) and selected single frames (B, D, F) are presented. In the wild-type gonad, SGPs extended numerous protrusions to ensheath PGCs (A, arrowheads in B). In ena mutants, SGPs appeared to have normal cytoplasmic extensions surrounding the PGCs (C, E, arrowheads in D, F). Some mutant SGPs, mostly in the anterior region, severely extend (arrows in E), resulting in an irregularly shaped gonad.

Figure Legend Snippet: (A–F) Wild-type and ena mutant embryos with the P six4 -egfp::moesin transgene were double stained with anti-GFP (green) and anti-Vas (magenta) antibodies. Labeled gonads at stages 15–16 were scanned and rendered into 3D images. Z projection (A, C, E) and selected single frames (B, D, F) are presented. In the wild-type gonad, SGPs extended numerous protrusions to ensheath PGCs (A, arrowheads in B). In ena mutants, SGPs appeared to have normal cytoplasmic extensions surrounding the PGCs (C, E, arrowheads in D, F). Some mutant SGPs, mostly in the anterior region, severely extend (arrows in E), resulting in an irregularly shaped gonad.

Techniques Used: Mutagenesis, Staining, Labeling

(A, B) The DE-cad protein in control and ena mutant embryos was detected by Western Blot (A) and the expression level of DE-cad normalized against α-tubulin expression was plotted in the graph (B). (C–H) Wild-type and ena mutant SGPs were stained with the DE-cad antibody, and the signal intensity on the outer membrane (red) or SGP-SGP boundary (blue) was measured (middle and left panels). The ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was calculated at stage 13 and stages 15–16 (middle panel). In wild type, DE-cad becomes enriched at the SGP-SGP boundary as gonad compaction proceeds (**P<0.01) (D–F). This process was affected in ena mutants (F–H). (I–K) Wild-type SGPs were stained with the anti-Ena antibody (I, J), and the ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was plotted at stage 13 and stages 15–16 (K). Ena localization shifts towards the SGP-SGP boundary at stages 15–16 (*P<0.05). The number of outer membranes versus SGP-SGP boundaries scored is indicated above the graph (F, K). Error bars in (B, F, and K) represent standard error.

Figure Legend Snippet: (A, B) The DE-cad protein in control and ena mutant embryos was detected by Western Blot (A) and the expression level of DE-cad normalized against α-tubulin expression was plotted in the graph (B). (C–H) Wild-type and ena mutant SGPs were stained with the DE-cad antibody, and the signal intensity on the outer membrane (red) or SGP-SGP boundary (blue) was measured (middle and left panels). The ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was calculated at stage 13 and stages 15–16 (middle panel). In wild type, DE-cad becomes enriched at the SGP-SGP boundary as gonad compaction proceeds (**P<0.01) (D–F). This process was affected in ena mutants (F–H). (I–K) Wild-type SGPs were stained with the anti-Ena antibody (I, J), and the ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was plotted at stage 13 and stages 15–16 (K). Ena localization shifts towards the SGP-SGP boundary at stages 15–16 (*P<0.05). The number of outer membranes versus SGP-SGP boundaries scored is indicated above the graph (F, K). Error bars in (B, F, and K) represent standard error.

Techniques Used: Mutagenesis, Western Blot, Expressing, Staining

other:

Article Title: Drosophila USP22/nonstop polarizes the actin cytoskeleton during collective border cell migration
Article Snippet: The following primary antibodies from the Developmental Studies Hybridoma Bank were used for immunostaining: mouse anti-Armadillo (N27A1, 1:200, concentrate), mouse anti-Enabled (5G2, 1:25, concentrate), mouse anti-β-gal (40-1a, 1:300, concentrate), mouse anti-Fasciclin 3 (7G10, 1:200, supernatant), mouse anti-Eyes Absent (eya10H6, 1:100, supernatant), and mouse anti-SCAR (P1C1, 1:200, concentrate).

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Journal: PLoS ONE

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

doi: 10.1371/journal.pone.0052649

Figure Lengend Snippet: (A–E) SGPs were detected by in situ hybridization with a 412 retrotransposon RNA probe (blue). PGCs were labeled with anti-Vasa (Vas) antibody (brown). The brown signal in a segmental pattern is β-galastosidase from the balancer chromosome. In wild type, individual SGP clusters align with PGCs at stage 13 (A) and undergo coalescence to form tightly associated embryonic gonads at stage 14 to 16 (B). In ena C14-06 mutants, individual SGP clusters fail or delay to adhere at stage 13, remaining instead in three clusters (arrows in C). Subsequently, mutant gonads fail to complete coalescence resulting in elongated (bracket in D) or split gonads (arrows in E). (F–H) Ena protein detected with anti-Ena antibody. Ena protein is expressed ubiquitously in the wild type (F). Ena protein was not detected in ena C14-06 mutants either by tissue-immuno fluorescence (G) or Western blotting (H). Scale bar in (A) represents 50 µm.

Article Snippet: Antibody staining was conducted as described previously , using the following primary antibodies: mouse anti-Ena (5G2, 1∶200; C. Goodman, DSHB), rabbit anti-Vas (1∶20,000; Lehmann, R.), chick anti-Vas (1∶300; Lehmann, R.), rabbit anti-Zfh-1 (1∶4,000; Lehmann, R.), rabbit anti-Serpent (1∶500; D. Hoshizaki), rabbit anti-GFP (1∶1,000; Clontech), rat anti-DE-cad (DCAD2, 1∶50; T. Uemura, DSHB).

Techniques: In Situ Hybridization, Labeling, Mutagenesis, Fluorescence, Western Blot

Journal: PLoS ONE

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

doi: 10.1371/journal.pone.0052649

Figure Lengend Snippet: (A–C) Stage-12 embryo stained with the anti-Ena antibody (magenta in A–B, white in C) and anti-Vas antibody to detect PGCs (green). The posterior half of the embryo is shown in (A), migrating PGCs are magnified in (B, C) (asterisks). Ena protein is found at the cell membranes (A) but not in migrating PGCs (B, C). (D–L) Ena expression during gonad coalescence. Wild-type embryos were stained with anti-Ena (magenta), anti-Zfh-1 antibodies, which mark the nuclei of the fat body and SGPs (green), and anti-Vas (PGCs in blue). Ena levels in the SGPs were indistinguishable from those in the surrounding tissues (D, high magnification in E, F). Ena expression in the SGPs was more pronounced in the mature gonad (G, J, high magnification in H–I and K–L). The scale bars in (A and D), (B), and (E) represent 50 µm, 10 µm, and 20 µm, respectively.

Techniques: Staining, Expressing

Journal: PLoS ONE

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

doi: 10.1371/journal.pone.0052649

Figure Lengend Snippet: (A–F) Rescue experiment of ena mutants. The coalescence phenotype at stages 15–16 was categorized into severe (green), intermediate (red), and normal classes (blue) as illustrated in (A), and number of gonads scored is indicated above the graph (B). Germline expression of Ena by nanos (nos) -Gal4 did not show any rescue activity (B) albeit the Ena protein derived from the transgene was detected in PGCs (blue in E and F). Ena expression in the mesoderm by 24B-Gal4 partially rescued the compaction phenotype in the mutants (B). (G–J) ena function was tested in a maternal oskar mutant background lacking PGCs. The 412 retrotransposon probe was used to label SGPs (blue). In maternal oskar mutants, SGPs were specified normally and compacted into spherical ‘gonads’ (G and H). In ena (zygotic), oskar (maternal) double mutants, SGP clusters failed to adhere at stage 13 (I), resulting in elongated gonads similar to those in zygotic ena mutants (J). (K–L) The stage-15 embryos were stained with anti-Serpent and anti-Vas antibodies to detect the fat body (magenta, bracket) and PGCs (green). The fat body appears unaffected by the ena mutation. Scale bars in (A) and (D) represent 50 µm.

Techniques: Expressing, Activity Assay, Derivative Assay, Mutagenesis, Staining

Journal: PLoS ONE

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

doi: 10.1371/journal.pone.0052649

Figure Lengend Snippet: (A–F) Wild-type and ena mutant embryos with the P six4 -egfp::moesin transgene were double stained with anti-GFP (green) and anti-Vas (magenta) antibodies. Labeled gonads at stages 15–16 were scanned and rendered into 3D images. Z projection (A, C, E) and selected single frames (B, D, F) are presented. In the wild-type gonad, SGPs extended numerous protrusions to ensheath PGCs (A, arrowheads in B). In ena mutants, SGPs appeared to have normal cytoplasmic extensions surrounding the PGCs (C, E, arrowheads in D, F). Some mutant SGPs, mostly in the anterior region, severely extend (arrows in E), resulting in an irregularly shaped gonad.

Techniques: Mutagenesis, Staining, Labeling

Journal: PLoS ONE

Article Title: The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis

doi: 10.1371/journal.pone.0052649

Figure Lengend Snippet: (A, B) The DE-cad protein in control and ena mutant embryos was detected by Western Blot (A) and the expression level of DE-cad normalized against α-tubulin expression was plotted in the graph (B). (C–H) Wild-type and ena mutant SGPs were stained with the DE-cad antibody, and the signal intensity on the outer membrane (red) or SGP-SGP boundary (blue) was measured (middle and left panels). The ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was calculated at stage 13 and stages 15–16 (middle panel). In wild type, DE-cad becomes enriched at the SGP-SGP boundary as gonad compaction proceeds (**P<0.01) (D–F). This process was affected in ena mutants (F–H). (I–K) Wild-type SGPs were stained with the anti-Ena antibody (I, J), and the ratio of the signal intensity on the outer membrane compared to that on the SGP-SGP boundary was plotted at stage 13 and stages 15–16 (K). Ena localization shifts towards the SGP-SGP boundary at stages 15–16 (*P<0.05). The number of outer membranes versus SGP-SGP boundaries scored is indicated above the graph (F, K). Error bars in (B, F, and K) represent standard error.

Techniques: Mutagenesis, Western Blot, Expressing, Staining

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mouse anti ena (Developmental Studies Hybridoma Bank)

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1) Product Images from "The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis"

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