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101.
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103.
Roles of the GLABROUS1 and TRANSPARENT TESTA GLABRA Genes in Arabidopsis Trichome Development 总被引:11,自引:5,他引:6
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Arabidopsis trichomes are branched, single-celled epidermal hairs. These specialized cells provide a convenient model for investigating the specification of cell fate in plants. Two key genes regulating the initiation of trichome development are GLABROUS1 (GL1) and TRANSPARENT TESTA GLABRA (TTG). GL1 is a member of the myb gene family. The maize R gene, which can functionally complement the Arabidopsis ttg mutation, encodes a basic helix-loop-helix protein. We used constitutively expressed copies of the GL1 and R genes to test hypotheses about the roles of GL1 and TTG in trichome development. The results support the hypothesis that TTG and GL1 cooperate at the same point in the trichome developmental pathway. Furthermore, the constitutive expression of both GL1 and R in the same plant caused trichomes to develop on all shoot epidermal surfaces. Results were also obtained indicating that TTG plays an additional role in inhibiting neighboring cells from becoming trichomes. 相似文献
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106.
We have evaluated codon usage bias in Drosophila histone genes and have
obtained the nucleotide sequence of a 5,161-bp D. hydei histone gene repeat
unit. This repeat contains genes for all five histone proteins (H1, H2a,
H2b, H3, and H4) and differs from the previously reported one by a second
EcoRI site. These D. hydei repeats have been aligned to each other and to
the 5.0-kb (i.e., long) and 4.8-kb (i.e., short) histone repeat types from
D. melanogaster. In each species, base composition at synonymous sites is
similar to the average genomic composition and approaches that in the small
intergenic spacers of the histone gene repeats. Accumulation of synonymous
changes at synonymous sites after the species diverged is quite high. Both
of these features are consistent with the relatively low codon usage bias
observed in these genes when compared with other Drosophila genes. Thus,
the generalization that abundantly expressed genes in Drosophila have high
codon bias and low rates of silent substitution does not hold for the
histone genes.
相似文献
107.
Vladimir Vartanian Jocelyn F. Krey Paroma Chatterjee Allison Curtis Makayla Six Sean P. M. Rice Sherri M. Jones Harini Sampath Charles N. Allen Renee C. Ryals R. Stephen Lloyd Peter G. Barr-Gillespie 《Genes, Brain & Behavior》2023,22(4):e12849
Relationships between novel phenotypic behaviors and specific genetic alterations are often discovered using target-specific, directed mutagenesis or phenotypic selection following chemical mutagenesis. An alternative approach is to exploit deficiencies in DNA repair pathways that maintain genetic integrity in response to spontaneously induced damage. Mice deficient in the DNA glycosylase NEIL1 show elevated spontaneous mutations, which arise from translesion DNA synthesis past oxidatively induced base damage. Several litters of Neil1 knockout mice included animals that were distinguished by their backwards-walking behavior in open-field environments, while maintaining frantic forward movements in their home cage environment. Other phenotypic manifestations included swim test failures, head tilting and circling. Mapping of the mutation that conferred these behaviors showed the introduction of a stop codon at amino acid 4 of the Ush1g gene. Ush1gbw/bw null mice displayed auditory and vestibular defects that are commonly seen with mutations affecting inner-ear hair-cell function, including a complete lack of auditory brainstem responses and vestibular-evoked potentials. As in other Usher syndrome type I mutant mouse lines, hair cell phenotypes included disorganized and split hair bundles, as well as altered distribution of proteins for stereocilia that localize to the tips of row 1 or row 2. Disruption to the bundle and kinocilium displacement suggested that USH1G is essential for forming the hair cell's kinocilial links. Consistent with other Usher type 1 models, Ush1gbw/bw mice had no substantial retinal degeneration compared with Ush1gbw/+ controls. In contrast to previously described Ush1g alleles, this new allele provides the first knockout model for this gene. 相似文献
108.
Taffet George E.; Michael Lloyd A.; Tate Charlotte A. 《Journal of applied physiology》1996,81(4):1488-1494
Taffet, George E., Lloyd A. Michael, and Charlotte A. Tate.Exercise training improves lusitropy by isoproterenol in papillarymuscles from aged rats. J. Appl.Physiol. 81(4): 1488-1494, 1996.Aging isassociated with a decreased cardiac responsiveness to -adrenergicstimulation. We examined the effect of endurance exercise training ofold Fischer 344 male rats on -adrenergic stimulation of the functionof isolated left ventricular papillary muscle. Three groups wereexamined: sedentary mature (SM; 12-mo old), sedentary old (SO;23-24 mo old), and exercised old (EO; 23-24 mo old) that weretreadmill trained for 4-8 wk. The isometric contractile propertieswere studied at 0.2 Hz and 0.75 mM calcium. Without -adrenergicstimulation, there were no group differences for peak tension, maximumrate of tension development(+dP/dt), or maximum rateof tension dissipation(dP/dt). The time to peak tension was longer (P < 0.05) forboth EO and SO than for SM rats. Half relaxation time(RT1/2) was prolonged(P < 0.05) for SO compared with SMand EO (which did not differ). The three groups did not differ in the-adrenergic stimulation by isoproterenol of peak tension,dP/dt, time to peak tension, orcontraction duration. The inotropic response(+dP/dt) of SM was greater(P < 0.05) than that in SO or EOrats (which did not differ); however, the lusitropic response(RT1/2) was lesser(P < 0.05) in SO than in SM or EO rats (which did not differ). Thus exercise training of old rats improved the lusitropic response to isoproterenol without altering theage-associated impairment in inotropic response. 相似文献
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110.
The SOS system of Escherichia coli aids survival following damage to DNA by promoting DNA repair while cell division is delayed. Induction of the SOS response is dependent on RecA and also on the product of recF. We show that normal induction also requires the products of recO and recR. SOS induction was monitored using a sfiA-lacZ fusion strain. Induction was delayed to a similar degree by mutation in recF, recO or recR. A similar effect was observed following overexpression of RecR from a recombinant recR
+plasmid. We show that the overexpression of RecR also reduces the UV resistance of a recBC sbcBC strain and of a sfiA strain, but not of a rec
+
sfiA
+strain. The implications of these data for the kinetics of DNA repair are discussed. 相似文献