Journal: bioRxiv
Article Title: A tunnel microtract organ for T cell progenitor homing is formed by neural crest morphogenesis via Sox10-Cdc42 axis
doi: 10.64898/2026.03.05.709688
Figure Lengend Snippet: a , Immunofluorescence images showing GFP + CD34 + mTMT encircling the thymus and extending cephalad to the thyroid cartilage. Enlarged views of white dashed boxes are shown in the right panels. b . Immunofluorescence images showing localization of IKZF1 + signals within GFP + mTMT across the anterior-dorsal (AD), anterior-ventral (AV), posterior-dorsal (PD), and posterior-ventral (PV) regions. Enlarged views of white dashed boxes are shown in the bottom panels. c , Quantification of the number of IKZF1 + signals in the AD, AV, PD, and PV regions of GFP + mTMT. d , Schematic illustration of preferential localization of T cells within mTMT. e, Immunofluorescence images showing morphology of GFP + mTMT (outlined by white dashed lines) in AD (top) and AV (bottom) regions at E12.5, E13.5, E14.5, and E15.5. f , Schematic illustration of the stereotyped morphogenetic program of mTMT from E12.5 to E15.5. g , Quantification of mTMT width in the AD and AV regions across developmental stages. h , Immunofluorescence images showing morphology of GFP + mTMT in the AD region of E15.5 Sox10 flox/flox and Wnt1 Cre/+ ; Sox10 flox/flox mouse thymus. i-k , Quantification of mTMT width ( i ), the number of CD34 + signals ( j ), and CD45 + signals ( k ) within mTMT in the AD regions of E15.5 Sox10 flox/flox and Wnt1 Cre/+ ; Sox10 flox/flox mouse thymus. tc, thyroid cartilage; as, anterior site. White and magenta arrowheads in h indicate the spindle-like and oval morphology of mTMT cells, respectively. Each dot in c , g , i-k represents one per section from three mice. Error bars represent mean ± SEM. Unpaired two-tailed Student’s t-test. P values are included in the graphs. The schematic diagrams in d , f , h were created with BioRender.com .
Article Snippet: The following mice were obtained from the Jackson laboratory: Wnt1 Cre ( H2az2 Tg(Wnt -cre)11Rth Tg(Wnt1-GAL4)11Rth/J, The Jackson Laboratory, 003829) , ROSA26 mT/mG (B6.129(Cg)- Gt(ROSA)26Sor tm4(ACTB-tdTomato,-EGFP)Luo/J , The Jackson Laboratory, 007676) , ROSA26 iDTR (C57BL/6- Gt(ROSA)26Sor tm1(HBEGF)Awai/J , The Jackson Laboratory, 007900) , Sox10 flox/flox (CKOCMP-20665-Sox10-B6J-VC, Cyagen Biosciences, S-CKO-17582) .
Techniques: Immunofluorescence, Two Tailed Test
Journal: bioRxiv
Article Title: Adrenergic signaling induces a pro-tumorigenic B cell state in colorectal cancer
doi: 10.64898/2026.01.23.700260
Figure Lengend Snippet: A| Timeline for AOM/DSS procedure to induce CRC, including timepoints at which CT scans were acquired. B| In vivo tumor tracking with CT scans shows no significant difference between Hand2 fl/+ ;Wnt1-Cre2 (N=12) and Hand2 fl/+ (N=12) mice in tumor burden. Tumor burden was calculated by summing all tumor volumes (mm³) per mouse. C| Hand2 fl/+ mice have significantly shorter colons than Hand2 fl/+ ;Wnt1-Cre2 mice. D| Tumor number, E| size (averaged per mouse, N=7 and N=8, mice without tumors were excluded from analysis) and F| burden (tumor number multiplied by average tumor size) are not significantly different between Hand2 fl/+ ;Wnt1-Cre2 and Hand2 fl/+ mice. G| There is no significant difference in relative frequency of the different tumor classifications between Hand2 fl/+ and Hand2 fl/+ ;Wnt1-Cre2 mice. H| Colon tumors were classified as hyperplasia (H), low grade adenoma (LGA), high grade adenoma (HGA), or adenocarcinoma (AC) based on histology. Scale bar is 100 µm. I| Volcano plot showing the mean log 2 -transformed fold change ( x -axis) and −log 10 -transformed P -value of differentially expressed genes between tumors from Hand2 fl/+ (N=3) and Hand2 fl/+ ;Wnt1-Cre2 (N=2) mice. Dashed lines indicate the threshold of significant gene expression, defined as log 2 -transformed fold change ≤−1 and ≥1 with −log 10 (P)≥1.301. J| The top 10 significantly decreased gene sets and all six significantly increased gene sets are shown with the normalized enrichment score. K| The top 15 significant biological pathways (-log 10 -transformed Q -value) from gene ontology analysis include ‘(defense) response to bacterium’ and ‘innate immune response’. L| GSEA was performed on hallmarks of cancer gene sets. The hallmarks ‘deregulating cellular energetics’ and ‘avoiding immune destruction’ were significantly enriched. All data are presented as mean ±SEM.
Article Snippet: To induce colitis-associated CRC, Hand2 fl/+ and Hand2 fl/+ ;Wnt1-Cre2 (10-12 weeks old males (unless otherwise specified)) were injected intraperitoneally with a single dose of 10 mg/kg of the carcinogen azoxymethane (AOM; sc-358746A, Santa-Cruz) dissolved in sterile phosphate-buffered saline (PBS).
Techniques: In Vivo, Transformation Assay, Gene Expression
Journal: bioRxiv
Article Title: Adrenergic signaling induces a pro-tumorigenic B cell state in colorectal cancer
doi: 10.64898/2026.01.23.700260
Figure Lengend Snippet: A| Analysis of lymphoid cells in the cancerous colon shows a significant reduction in the number of B cells in Hand2 fl/+ ;Wnt1-Cre2 (N=7) compared to Hand2 fl/+ (N=4) mice. B| Myeloid cells are not affected by hypo-innervation. C| Flow cytometry plots of B cells D| and germinal center (GC) B cells depict the decrease in population abundance in Hand2 fl/+ ;Wnt1-Cre2 mice. E| B cell subtype analysis identifies the specific downregulation of GC B cells and immature B cells in hypo-innervated cancerous colon (N=8) compared to control cancerous colon (N=8). F| Immunoglobulin expression on B cells is altered by an increase in IgD + and a decrease in IgA + B cells. G| In healthy colon, no differences in lymphoid populations were observed in Hand2 fl/+ ;Wnt1-Cre2 (N=8) compared to Hand2 fl/+ (N=8) mice. H| B cell subtype analysis shows a shift towards more mature B cells in hypo-innervated colon, but GC B cells are not affected. I| Relative abundance of immunoglobulin-expressing B cells remains unaltered. In inflamed colons (N=8 vs 8), J| lymphoid populations, K| B cell subtypes, and L| Ig-expressing B cells are not affected by a decreased neuronal density. All data are presented as mean ±SEM.
Article Snippet: To induce colitis-associated CRC, Hand2 fl/+ and Hand2 fl/+ ;Wnt1-Cre2 (10-12 weeks old males (unless otherwise specified)) were injected intraperitoneally with a single dose of 10 mg/kg of the carcinogen azoxymethane (AOM; sc-358746A, Santa-Cruz) dissolved in sterile phosphate-buffered saline (PBS).
Techniques: Flow Cytometry, Control, Expressing
Journal: bioRxiv
Article Title: Adrenergic signaling induces a pro-tumorigenic B cell state in colorectal cancer
doi: 10.64898/2026.01.23.700260
Figure Lengend Snippet: A| B cells (↑brown, ↓red) are located in close proximity to neuronal processes (↑red, ↓green) in the submucosal layer of the colon as single cells, or B| as lymphoid clusters. C| In AOM/DSS-treated Hand2 fl/+ ;Wnt1-Cre2 mice, B cells are also present in the tumor stroma in vicinity of nerve fibers. Scale bars are 100 µm. D| Electron microscopy imaging confirms the close proximity of nerve fibers (green) and B cells (red) in human CRC tissues, and neurotransmitter vesicles are observed in fibers neighboring B cells (arrows). Scale bars are 1 µm and 500 nm. E| The colonic B cells of Hand2 fl/+ and Hand2 fl/+ ;Wnt1-Cre2 mice express cholinergic (Chrn/Chrm), adrenergic (Adr) and VIPergic (Vipr) receptor family members (N=6), with no effect of innervation level on neurotransmitter receptor profile.
Article Snippet: To induce colitis-associated CRC, Hand2 fl/+ and Hand2 fl/+ ;Wnt1-Cre2 (10-12 weeks old males (unless otherwise specified)) were injected intraperitoneally with a single dose of 10 mg/kg of the carcinogen azoxymethane (AOM; sc-358746A, Santa-Cruz) dissolved in sterile phosphate-buffered saline (PBS).
Techniques: Electron Microscopy, Imaging
Fig. S2A for anatomical landmarks) and pN3 WT and mutant PF (E) and Sag (F) sutures. (D) Decreased proliferative activity in surface ectoderm and adjacent mesenchymal layers of mutant compared to WT E9.5 head area (arrows). (E,F) Decreased PCNA staining in mutant compared to WT PF and Sag suture mesenchyme, periosteum and dura mater and similar activity in bone fronts (dashed lines). Negative control for PCNA without primary antibody is shown in the bottom panels of F. (G) Scratch assay to assess in vitro migration of dura mater cells and osteoblasts from WT and Sh3Pxd2b nee−/− mice at 0 and 24 h, demonstrating decreased migration in mutant dura mater cells. Dashed boxes indicate scratch area reducing over time. (H) Summary line graphs quantifying cell migration as percentage of decrease of initial scratch area. Significantly decreased migration is observed in mutant compared to WT dura mater (DM) cells. Migration in WT and mutant osteoblasts (Ob) is similar. (I) Quantification of dura mater cells and osteoblasts with podosome formation with/without TGFβ as a percentage of all counted cells showing significantly decreased number of dura mater cells with podosome formation mutant compared to WT mice, upon TGFβ stimulation (left graph), and significantly decreased number of osteoblasts with podosome formation in stimulated and unstimulated mutant compared to WT cells (right graph). (J,K) Immunocytochemistry for cortactin, F-actin and DAPI in dura mater cells and osteoblasts with/without TGFβ from WT and Sh3Pxd2b nee−/− mice. Boxed areas showing regions of interest are shown at higher magnification on the right. (J) Increased perinuclear accumulation is observed in unstimulated WT cells (arrowheads, magnified panel). Upon TGFβ stimulation in WT cells, cortactin spreads out in the cytoplasm. Actin-rich puncta colocalize with cortactin as indicated by yellow staining, localized in small clusters near the cell membranes and in cell protrusions of stimulated WT cells (arrows, magnified panel). In mutant unstimulated cells, cortactin accumulates in perinuclear regions (arrowheads, magnified panel). Cell membranes appear frayed. Upon TGFβ stimulation, cortactin colocalizes with actin at the cell membranes (arrows, magnified panel). (K) In WT osteoblasts, intense cortactin staining is observed along the cell membranes (arrowheads, magnified panel). Upon TGFβ stimulation, cortactin spreads out in the cytoplasm towards large cell protrusions with multiple actin-rich puncta colocalizing with cortactin (arrows, magnified panel). In unstimulated and stimulated mutant osteoblasts, cortactin accumulates in perinuclear regions (arrowheads). Small puncta form unevenly distributed in the cytoplasm but do not colocalize with actin and do not accumulate near the cell membrane (arrow). Cell protrusions do not form. (L) Schematic depicting creation of calvarial defects in mouse parietal bones and harvesting of skulls at 0, 24 and 48 h postoperatively. Created in BioRender by Huber, J., 2026. https://BioRender.com/h47f781 . This figure was sublicensed under CC BY 4.0 terms. (M) Hematoxylin and Eosin-stained 10 µm sections of representative calvarial defect area in WT and Sh3Pxd2b nee−/− mice at 0, 24 and 48 h postoperatively. At 24 and 48 h, cells have migrated into the defect area in WT mice, whereas in mutant mice no migration of cells can be observed. See also
Fig. S3 . (N) 10 µm sections of representative calvarial defect area in Wnt1-Cre2 +/− ;mT/mG and Wnt1-Cre2 +/− ;mT/mG;Sh3Pxd2b nee−/− mice showing migration of Wnt1-Cre2-positive cells expressing green fluorescent protein into the defect area in WT mice and no migration in mutant calvarial defects, respectively. In M and N, dura mater is marked with green arrows and migration area with blue dashed lines. Experiments were performed in triplicate with n =3 per group, when applicable. Data shown as mean (±s.d.). * P <0.05; ** P <0.01 (ANOVA, Šidák's multiple comparisons). " width="100%" height="100%">
Journal: Development (Cambridge, England)
Article Title: The Sh3Pxd2b nee−/− mouse reveals developmental features of Frank-ter Haar syndrome
doi: 10.1242/dev.204631
Figure Lengend Snippet: Sh3Pxd2b nee−/− mice are characterized by decreased proliferation and migration in vitro and in vivo . (A,B) EdU proliferation assay shows decreased proliferation in mutant (bottom) dura mater cells (A) and osteoblasts (B) compared to WT cells (top). (C) Percentage of EdU-positive WT and mutant osteoblasts and dura mater cells. (D-F) Immunofluorescence staining for PCNA in the presumptive head area of E9.5 (D; see Fig. S2A for anatomical landmarks) and pN3 WT and mutant PF (E) and Sag (F) sutures. (D) Decreased proliferative activity in surface ectoderm and adjacent mesenchymal layers of mutant compared to WT E9.5 head area (arrows). (E,F) Decreased PCNA staining in mutant compared to WT PF and Sag suture mesenchyme, periosteum and dura mater and similar activity in bone fronts (dashed lines). Negative control for PCNA without primary antibody is shown in the bottom panels of F. (G) Scratch assay to assess in vitro migration of dura mater cells and osteoblasts from WT and Sh3Pxd2b nee−/− mice at 0 and 24 h, demonstrating decreased migration in mutant dura mater cells. Dashed boxes indicate scratch area reducing over time. (H) Summary line graphs quantifying cell migration as percentage of decrease of initial scratch area. Significantly decreased migration is observed in mutant compared to WT dura mater (DM) cells. Migration in WT and mutant osteoblasts (Ob) is similar. (I) Quantification of dura mater cells and osteoblasts with podosome formation with/without TGFβ as a percentage of all counted cells showing significantly decreased number of dura mater cells with podosome formation mutant compared to WT mice, upon TGFβ stimulation (left graph), and significantly decreased number of osteoblasts with podosome formation in stimulated and unstimulated mutant compared to WT cells (right graph). (J,K) Immunocytochemistry for cortactin, F-actin and DAPI in dura mater cells and osteoblasts with/without TGFβ from WT and Sh3Pxd2b nee−/− mice. Boxed areas showing regions of interest are shown at higher magnification on the right. (J) Increased perinuclear accumulation is observed in unstimulated WT cells (arrowheads, magnified panel). Upon TGFβ stimulation in WT cells, cortactin spreads out in the cytoplasm. Actin-rich puncta colocalize with cortactin as indicated by yellow staining, localized in small clusters near the cell membranes and in cell protrusions of stimulated WT cells (arrows, magnified panel). In mutant unstimulated cells, cortactin accumulates in perinuclear regions (arrowheads, magnified panel). Cell membranes appear frayed. Upon TGFβ stimulation, cortactin colocalizes with actin at the cell membranes (arrows, magnified panel). (K) In WT osteoblasts, intense cortactin staining is observed along the cell membranes (arrowheads, magnified panel). Upon TGFβ stimulation, cortactin spreads out in the cytoplasm towards large cell protrusions with multiple actin-rich puncta colocalizing with cortactin (arrows, magnified panel). In unstimulated and stimulated mutant osteoblasts, cortactin accumulates in perinuclear regions (arrowheads). Small puncta form unevenly distributed in the cytoplasm but do not colocalize with actin and do not accumulate near the cell membrane (arrow). Cell protrusions do not form. (L) Schematic depicting creation of calvarial defects in mouse parietal bones and harvesting of skulls at 0, 24 and 48 h postoperatively. Created in BioRender by Huber, J., 2026. https://BioRender.com/h47f781 . This figure was sublicensed under CC BY 4.0 terms. (M) Hematoxylin and Eosin-stained 10 µm sections of representative calvarial defect area in WT and Sh3Pxd2b nee−/− mice at 0, 24 and 48 h postoperatively. At 24 and 48 h, cells have migrated into the defect area in WT mice, whereas in mutant mice no migration of cells can be observed. See also Fig. S3 . (N) 10 µm sections of representative calvarial defect area in Wnt1-Cre2 +/− ;mT/mG and Wnt1-Cre2 +/− ;mT/mG;Sh3Pxd2b nee−/− mice showing migration of Wnt1-Cre2-positive cells expressing green fluorescent protein into the defect area in WT mice and no migration in mutant calvarial defects, respectively. In M and N, dura mater is marked with green arrows and migration area with blue dashed lines. Experiments were performed in triplicate with n =3 per group, when applicable. Data shown as mean (±s.d.). * P <0.05; ** P <0.01 (ANOVA, Šidák's multiple comparisons).
Article Snippet: Wnt1-Cre2 mice and mT/mG mice were purchased from The Jackson Laboratory ( ; ; ).
Techniques: Migration, In Vitro, In Vivo, Proliferation Assay, Mutagenesis, Immunofluorescence, Staining, Activity Assay, Negative Control, Wound Healing Assay, Immunocytochemistry, Membrane, Expressing
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