Ask about this productRelated genes to: LEFTY1 Blocking Peptide
- Gene:
- LEFTY1 NIH gene
- Name:
- left-right determination factor 1
- Previous symbol:
- LEFTB
- Synonyms:
- LEFTYB
- Chromosome:
- 1q42.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-09
- Date modifiied:
- 2016-10-05
Related products to: LEFTY1 Blocking Peptide
Related articles to: LEFTY1 Blocking Peptide
- Colorectal cancer (CRC) remains a leading cause of cancer‑related morbidity and mortality worldwide. Although the adenoma-carcinoma sequence and its genetic drivers are well described, the earliest cellular and molecular events initiating tumorigenesis within histologically normal colonic epithelium remain poorly defined. This study aims to identify tumor‑initiating cells (TICs), distinguish them from normal stem‑like cells (nSTMs), and delineate early transcriptional and signaling programs using single‑cell RNA sequencing (scRNA‑seq) from paired normal‑appearing and transformed human colonic tissues. - Source: PubMed
Publication date: 2026/03/27
Jaiswal SangeetaThe StephanieChang Tse-ShaoShi JiaqiWang Thomas D - The cardiac conduction system (CCS) develops asymmetrically along the body axes. In heterotaxy syndrome - resulting from aberrant left-right axis formation - atrial and atrioventricular conduction defects can cause life-threatening arrhythmias. However, the developmental mechanisms regulating the atrioventricular conduction system (AVCS) disposition and integrity remain unclear. To investigate the etiology of AVCS malformations in laterality defects, we analyzed CCS development and function in mouse mutants for Cryptic and Lefty1, which are key regulators of Pitx2 in the left-right axis formation. Cryptic-/- embryos exhibited bilateral sinoatrial nodes and an ectopic anterior AV node and bundle accompanied by reduced Pitx2 expression. In contrast, Lefty1-/- embryos showed a hypoplastic sinoatrial node and AV node-bundle dissociation with ectopic Pitx2 expression. Single-cell transcriptomic analysis of Pitx2-/- hearts revealed expansion of AV node and bundle populations, consistent with a repressive role of Pitx2 in AVCS specification. Genetic lineage tracing indicated that Pitx2-expressing cells from the left lateral plate mesoderm populate cranioventral cardiac regions, where AVCS development is suppressed. Together, these findings clarify how global left-right axis information is locally integrated to shape AVCS disposition and integrity, providing a mechanistic model for AVCS abnormalities in laterality-associated congenital heart disease. - Source: PubMed
Publication date: 2026/02/24
Joo KunihikoMatsuoka RyoheiKitajima KeikoYashiro KentaShiose AkiraTominaga RyujiShen Michael MOki ShinyaMeno Chikara - Colorectal cancer (CRC) remains a major cause of cancer-related morbidity and mortality worldwide. Although the adenoma-carcinoma sequence and associated genetic alterations are well characterized, the earliest cellular and molecular events that initiate tumorigenesis within histologically normal colonic epithelium remain poorly defined. This study aims to identify tumor-initiating cells (TICs) and early transcriptional markers of neoplastic transformation using single-cell RNA sequencing (scRNA-seq) from paired normal-appearing and transformed human colonic tissues. - Source: PubMed
Publication date: 2025/10/27
Jaiswal SangeetaThe StephanieChang Tse-ShaoShi JiaqiWang Thomas D - Mammalian primordial germ cells (PGCs) migrate asynchronously through the embryonic hindgut and dorsal mesentery to reach the gonads. We previously found that interaction with different somatic niches regulates mouse PGC proliferation along the migration route. To characterize transcriptional heterogeneity of migrating PGCs and their niches, we performed single-cell RNA sequencing of 13,262 mouse PGCs and 7868 surrounding somatic cells during migration (E9.5, E10.5, E11.5) and in anterior vs posterior locations to enrich for leading and lagging migrants. Analysis of PGCs by position revealed dynamic gene expression changes between faster or earlier migrants in the anterior and slower or later migrants in the posterior at E9.5; these differences include migration-associated actin polymerization machinery and epigenetic reprogramming-associated genes. We furthermore identified changes in signaling with various somatic niches, notably strengthened interactions with hindgut epithelium via non-canonical WNT (ncWNT) in posterior PGCs compared to anterior. Reanalysis of a previously published dataset suggests that ncWNT signaling from the hindgut epithelium to early migratory PGCs is conserved in humans. Trajectory inference methods identified putative differentiation trajectories linking cell states across timepoints and from posterior to anterior in our mouse dataset. At E9.5, we mainly observed differences in cell adhesion and actin cytoskeletal dynamics between E9.5 posterior and anterior migrants. At E10.5, we observed divergent gene expression patterns between putative differentiation trajectories from posterior to anterior, including Nodal signaling response genes and and reprogramming factors and . At E10.5, we experimentally validated anterior migrant-specific upregulation via whole-mount immunofluorescence staining for LEFTY1/2 and phosphorylated SMAD2/3, suggesting that elevated autocrine Nodal signaling in migrating PGCs occurs as they near the gonadal ridges. Together, this positional and temporal atlas of mouse PGCs supports the idea that niche interactions along the migratory route elicit changes in proliferation, actin dynamics, pluripotency, and epigenetic reprogramming. - Source: PubMed
Publication date: 2025/11/19
Jaszczak Rebecca GarrettZussman Jay WWagner Daniel ELaird Diana J - Cfap298 is a highly conserved gene required for ciliary motility and dynein arm assembly, with known roles in left-right (LR) patterning in zebrafish and links to human ciliopathies. Here, we describe a Cfap298 mutant allele, Cfap298ΔΔS, which selectively disrupts LR axis establishment in mice. Mutant embryos display organ laterality defects and abnormal Nodal, Pitx2 and Lefty1 expression, consistent with an early disruption in LR symmetry breaking. LR asymmetry is established by leftward fluid flow in the node, generated by planar-polarized cilia. Although cfap298 mutations are reported to affect planar polarity, we did not observe changes in cilia position, length or CELSR1 localization within the node, suggesting that Cfap298ΔΔS functions at the level of cilia motility. Accordingly, cilia lining the trachea of Cfap298ΔΔS mutants fail to beat or beat incorrectly. Expression of the Cfap298ΔΔS variant in zebrafish partially rescues body curvature defects but fails to rescue LR defects of cfap298 (kurly) loss-of-function mutants. These results confirm a conserved role for Cfap298 in mammalian LR patterning and identify a previously unreported region of CFAP298 with a conserved and essential role in cilia motility. - Source: PubMed
Publication date: 2025/10/31
Cortez MarvinYoung Cullen BLittle Katherine AGrimes Daniel TDevenport DanelleBurdine Rebecca D