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Deletion of Snai2 and Snai3 results in impaired physical development compounded by lymphocyte deficiency.

Pioli PD, Dahlem TJ, Weis JJ, Weis JH - PLoS ONE (2013)

Bottom Line: Less is known about the third member of the family, Snai3.Utilizing Cre-mediated deletion to facilitate the ablation of Snai3 in T cells or the entire animal, we found little to no effect of the loss of Snai3 in the entire animal or in T cell lineages.This finding provided the hypothesis that absence of Snai3 was mitigated, in part, by the presence of Snai2.

View Article: PubMed Central - PubMed

Affiliation: The Division of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, United States of America.

ABSTRACT
The Snail family of transcriptional regulators consists of three highly conserved members. These proteins regulate (repress) transcription via the recruitment of histone deacetylases to target gene promoters that possess the appropriate E-box binding sequences. Murine Snai1 is required for mouse development while Snai2 deficient animals survive with some anomalies. Less is known about the third member of the family, Snai3. To investigate the function of Snai3, we generated a conditional knockin mouse. Utilizing Cre-mediated deletion to facilitate the ablation of Snai3 in T cells or the entire animal, we found little to no effect of the loss of Snai3 in the entire animal or in T cell lineages. This finding provided the hypothesis that absence of Snai3 was mitigated, in part, by the presence of Snai2. To test this hypothesis we created Snai2/Snai3 double deficient mice. The developmental consequences of lacking both of these proteins was manifested in stunted growth, a paucity of offspring including a dramatic deficiency of female mice, and impaired immune cell development within the lymphoid lineages.

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Snai2 and Snai3 DKO lymphoid organs are reduced in size but present a healthy appearance.(A) Representative photo of thymus, spleen, and bone marrow dissected from age and sex matched WT and DKO animals. Organs are presented with a ruler for reference. (B–C) Quantification of thymic (B) and splenic (C) mass among different iterations of Snai2 and Snai3 knockouts. % of Body Mass = (Organ Weight (mg) / Body Weight (mg)) X 100, One-way ANOVA with Bonferroni post hoc test: * p < 0.05.
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pone-0069216-g006: Snai2 and Snai3 DKO lymphoid organs are reduced in size but present a healthy appearance.(A) Representative photo of thymus, spleen, and bone marrow dissected from age and sex matched WT and DKO animals. Organs are presented with a ruler for reference. (B–C) Quantification of thymic (B) and splenic (C) mass among different iterations of Snai2 and Snai3 knockouts. % of Body Mass = (Organ Weight (mg) / Body Weight (mg)) X 100, One-way ANOVA with Bonferroni post hoc test: * p < 0.05.

Mentions: Next we examined various lymphoid organs for gross morphology. The thymus, spleen and bone structure from DKO mice had a normal outward appearance (Figure 6A) although the sizes of the lymphoid organs were smaller in the DKO animal. When normalized to body weight, the DKO thymus was significantly smaller compared to WT (Figure 6B). No significant changes were seen in splenic mass between WT and DKO animals (Figure 6C). Additionally, Snai2+/- Snai3-/- and Snai2-/- Snai3+/- mice had organ masses comparable to WT mice.


Deletion of Snai2 and Snai3 results in impaired physical development compounded by lymphocyte deficiency.

Pioli PD, Dahlem TJ, Weis JJ, Weis JH - PLoS ONE (2013)

Snai2 and Snai3 DKO lymphoid organs are reduced in size but present a healthy appearance.(A) Representative photo of thymus, spleen, and bone marrow dissected from age and sex matched WT and DKO animals. Organs are presented with a ruler for reference. (B–C) Quantification of thymic (B) and splenic (C) mass among different iterations of Snai2 and Snai3 knockouts. % of Body Mass = (Organ Weight (mg) / Body Weight (mg)) X 100, One-way ANOVA with Bonferroni post hoc test: * p < 0.05.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3713067&req=5

pone-0069216-g006: Snai2 and Snai3 DKO lymphoid organs are reduced in size but present a healthy appearance.(A) Representative photo of thymus, spleen, and bone marrow dissected from age and sex matched WT and DKO animals. Organs are presented with a ruler for reference. (B–C) Quantification of thymic (B) and splenic (C) mass among different iterations of Snai2 and Snai3 knockouts. % of Body Mass = (Organ Weight (mg) / Body Weight (mg)) X 100, One-way ANOVA with Bonferroni post hoc test: * p < 0.05.
Mentions: Next we examined various lymphoid organs for gross morphology. The thymus, spleen and bone structure from DKO mice had a normal outward appearance (Figure 6A) although the sizes of the lymphoid organs were smaller in the DKO animal. When normalized to body weight, the DKO thymus was significantly smaller compared to WT (Figure 6B). No significant changes were seen in splenic mass between WT and DKO animals (Figure 6C). Additionally, Snai2+/- Snai3-/- and Snai2-/- Snai3+/- mice had organ masses comparable to WT mice.

Bottom Line: Less is known about the third member of the family, Snai3.Utilizing Cre-mediated deletion to facilitate the ablation of Snai3 in T cells or the entire animal, we found little to no effect of the loss of Snai3 in the entire animal or in T cell lineages.This finding provided the hypothesis that absence of Snai3 was mitigated, in part, by the presence of Snai2.

View Article: PubMed Central - PubMed

Affiliation: The Division of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, United States of America.

ABSTRACT
The Snail family of transcriptional regulators consists of three highly conserved members. These proteins regulate (repress) transcription via the recruitment of histone deacetylases to target gene promoters that possess the appropriate E-box binding sequences. Murine Snai1 is required for mouse development while Snai2 deficient animals survive with some anomalies. Less is known about the third member of the family, Snai3. To investigate the function of Snai3, we generated a conditional knockin mouse. Utilizing Cre-mediated deletion to facilitate the ablation of Snai3 in T cells or the entire animal, we found little to no effect of the loss of Snai3 in the entire animal or in T cell lineages. This finding provided the hypothesis that absence of Snai3 was mitigated, in part, by the presence of Snai2. To test this hypothesis we created Snai2/Snai3 double deficient mice. The developmental consequences of lacking both of these proteins was manifested in stunted growth, a paucity of offspring including a dramatic deficiency of female mice, and impaired immune cell development within the lymphoid lineages.

Show MeSH
Related in: MedlinePlus