PUBLICATION

Heart and gut chiralities are controlled independently from initial heart position in the developing zebrafish

Authors
Chin, A.J., Tsang, M., and Weinberg, E.S.
ID
ZDB-PUB-001205-15
Date
2000
Source
Developmental Biology   227(2): 403-421 (Journal)
Registered Authors
Chin, Alvin J., Tsang, Michael, Weinberg, Eric
Keywords
left-right axis; heart looping; gut chirality; heterotaxy; zebrafish
MeSH Terms
  • Transforming Growth Factor beta/genetics
  • Nuclear Proteins*
  • Body Patterning/genetics
  • Models, Biological
  • Mesoderm/cytology
  • Heart/embryology*
  • In Situ Hybridization
  • Animals
  • Digestive System/embryology*
  • Zebrafish Proteins*
  • Left-Right Determination Factors
  • Mutation
  • Paired Box Transcription Factors
  • Transcription Factors/genetics
  • Humans
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Homeodomain Proteins/genetics
  • Gene Expression Regulation, Developmental
(all 19)
PubMed
11071763 Full text @ Dev. Biol.
Abstract
A fundamental problem in developmental biology is how left-right (LR) asymmetry is generated, both on the whole organism level and at the level of an individual organ or structure. To investigate the relationship of organ sidedness to organ chirality, we examined 12 zebrafish mutants for initial heart tube position and later heart looping direction (chirality). Anomalous initial heart position was found in seven mutants, which also demonstrated loss of normal LR asymmetry in lateral plate mesoderm (LPM) antivin/lefty-1 and Pitx2 expression. Those with a relatively normal notochord (cyc(b16), din, and spt) displayed a predictive correlation between initial heart position and heart chirality, whereas initial heart position and heart chirality were independently randomized in those with a defective notochord (flh, boz, ntl, and mom). The predictability of heart chirality in spt, din, and b16 embryos, even in the absence of normal antivin/lefty-1 and Pitx2 expression, strongly suggests that heart chirality is controlled by a process distinct from that which controls appropriate left-sided LPM expression of antivin-Pitx2 signaling pathway molecules. In addition, there was correlation of initial heart position with gut chirality (and also between heart chirality and gut chirality) in the first class of mutants with normal notochord, but not in the second class, which appears to model human heterotaxy syndrome.
Genes / Markers
Figures
Figure Gallery (4 images)
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b16
    		Deficiency
    b104
      		Indel
      b160
        		Indel
        m168
          		Point Mutation
          n1
            		Small Deletion
            tc41
              		Unknown
              th211
                		Unknown
                tm41
                  		Unknown
                  tt250
                    		Point Mutation
                    1 - 9 of 9
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                    Human Disease / Model
                    No data available
                    Sequence Targeting Reagents
                    No data available
                    Fish
                    Fish
                    chrdtt250/tt250
                    Df(Chr12:hhex,ndr2)b16/b16 (AB)
                    dharmam168/m168 (AB)
                    dharmath211/th211
                    noton1/n1 (AB)
                    tbx16b104/b104 (AB)
                    tbx16tm41/tm41
                    tbxtab160/b160 (AB)
                    tbxtatc41/tc41
                    1 - 9 of 9
                    Show
                    Antibodies
                    No data available
                    Orthology
                    No data available
                    Engineered Foreign Genes
                    No data available
                    Mapping
                    No data available
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                    Citation
                    Chin, A.J., Tsang, M., and Weinberg, E.S. (2000) Heart and gut chiralities are controlled independently from initial heart position in the developing zebrafish. Developmental Biology. 227(2):403-421.