CRABS CLAW, a gene that regulates carpel and nectary development in Arabidopsis, encodes a novel protein with zinc finger and helix-loop-helix domains

Development ◽  
1999 ◽  
Vol 126 (11) ◽  
pp. 2387-2396 ◽  
Author(s):  
J.L. Bowman ◽  
D.R. Smyth

Studies of plants with mutations in the CRABS CLAW gene indicate that it is involved in suppressing early radial growth of the gynoecium and in promoting its later elongation. It is also required for the initiation of nectary development. To gain further insight, the gene was cloned by chromosome walking. CRABS CLAW encodes a putative transcription factor containing a zinc finger and a helix-loop-helix domain. The latter resembles the first two helices of the HMG box, known to bind DNA. At least five other genes of Arabidopsis carry the same combination of domains, and we have named them the yabby family. The new helix-loop-helix domain itself we call the yabby domain. Consistent with the mutant phenotype, CRABS CLAW expression is mostly limited to carpels and nectaries. It is expressed in gynoecial primordia from their inception, firstly in lateral sectors where it may inhibit radial growth, and later in the epidermis and in four internal strips. The internal expression may be sufficient to support longitudinal growth, as carpels are longer in a crabs claw promoter mutant where expression is now confined to these regions. The patterns of expression of CRABS CLAW in ectopic carpels of floral homeotic mutants suggest that it is negatively regulated by the A and B organ identity functions, but largely independent of C function. CRABS CLAW expression occurs in nectaries throughout their growth and maturation. It is also expressed in their presumptive anlagen so it may specify cells that will later develop as nectaries. Nectaries arise from the floral receptacle at normal positions in all A, B and C organ identity mutants examined, and CRABS CLAW is always expressed within them. Thus CRABS CLAW expression is regulated independently in carpels and nectaries.

Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1327-1333 ◽  
Author(s):  
PD Aplan ◽  
DP Lombardi ◽  
GH Reaman ◽  
HN Sather ◽  
GD Hammond ◽  
...  

Abstract The SCL gene, initially discovered at the site of a translocation breakpoint associated with the development of a stem cell leukemia, encodes a protein that contains the highly conserved basic helix-loop- helix (bHLH) motif found in a large array of eukaryotic transcription factors. Recently, we have described a nonrandom, site-specific SCL rearrangement in several T-cell acute lymphoblastic leukemia (ALL) cell lines that juxtaposes SCL with a distinct transcribed locus, SIL. The SIL/SCL rearrangement was found in leukemic blasts from 11 of 70 (16%) newly diagnosed T-cell ALL patients, a prevalence substantially higher than that of the t(11;14) translocation, which has previously been reported as the most frequent nonrandom chromosomal abnormality in T- cell ALL. We did not detect the SIL/SCL rearrangement in the leukemic blasts from 30 patients with B-cell precursor ALL, indicating that the rearrangement was specific for T-cell ALL. Analysis of RNA from these patients indicated that an SIL/SCL fusion mRNA was formed, joining SIL and SCL in a head-to-tail fashion. The fusion occurs in the 5′ untranslated region (UTR) of both genes, preserving the SCL coding region. The net result of this rearrangement is that SCL mRNA expression becomes regulated by the SIL promoter, leading to inappropriate SCL expression. The resultant inappropriate expression of this putative transcription factor may then contribute to leukemic transformation in T-cell ALL.


1990 ◽  
Vol 10 (8) ◽  
pp. 4384-4388 ◽  
Author(s):  
C S Carr ◽  
P A Sharp

A human cDNA encoding a novel protein in the helix-loop-helix family has been isolated by screening a bacteriophage expression library with a probe containing the binding site for major late transcription factor. The protein encoded by this cDNA, TFEB, probably recognizes E-box sequences in the heavy-chain immunoglobulin enhancer.


1990 ◽  
Vol 10 (8) ◽  
pp. 4384-4388
Author(s):  
C S Carr ◽  
P A Sharp

A human cDNA encoding a novel protein in the helix-loop-helix family has been isolated by screening a bacteriophage expression library with a probe containing the binding site for major late transcription factor. The protein encoded by this cDNA, TFEB, probably recognizes E-box sequences in the heavy-chain immunoglobulin enhancer.


Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3123-3134 ◽  
Author(s):  
T. Klein ◽  
J.A. Campos-Ortega

The klumpfuss (klu) transcription unit in Drosophila gives rise to two different transcripts of 4.5 and 4.9 kb, both of which encode a putative transcription factor with four zinc-finger motifs of the C2H2 class. Zinc-finger 2–4 are homologous to those of the proteins of the EGR transcription factor family. As in the case of the most divergent member of the family, the Wilms' tumor suppressor gene (WT-1), klu contains an additional zinc finger, which is only distantly related. Loss of klumpfuss function is semilethal and causes a variety of defects in bristles and legs of adults, as well as in mouth hooks and brains of larvae. Analysis of the mutants indicates that klumpfuss is required for proper specification and differentiation of a variety of cells, including the sensory organ mother cells and those of the distal parts of tarsal segments.


Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1327-1333 ◽  
Author(s):  
PD Aplan ◽  
DP Lombardi ◽  
GH Reaman ◽  
HN Sather ◽  
GD Hammond ◽  
...  

The SCL gene, initially discovered at the site of a translocation breakpoint associated with the development of a stem cell leukemia, encodes a protein that contains the highly conserved basic helix-loop- helix (bHLH) motif found in a large array of eukaryotic transcription factors. Recently, we have described a nonrandom, site-specific SCL rearrangement in several T-cell acute lymphoblastic leukemia (ALL) cell lines that juxtaposes SCL with a distinct transcribed locus, SIL. The SIL/SCL rearrangement was found in leukemic blasts from 11 of 70 (16%) newly diagnosed T-cell ALL patients, a prevalence substantially higher than that of the t(11;14) translocation, which has previously been reported as the most frequent nonrandom chromosomal abnormality in T- cell ALL. We did not detect the SIL/SCL rearrangement in the leukemic blasts from 30 patients with B-cell precursor ALL, indicating that the rearrangement was specific for T-cell ALL. Analysis of RNA from these patients indicated that an SIL/SCL fusion mRNA was formed, joining SIL and SCL in a head-to-tail fashion. The fusion occurs in the 5′ untranslated region (UTR) of both genes, preserving the SCL coding region. The net result of this rearrangement is that SCL mRNA expression becomes regulated by the SIL promoter, leading to inappropriate SCL expression. The resultant inappropriate expression of this putative transcription factor may then contribute to leukemic transformation in T-cell ALL.


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