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Biomedical subjects

M Terzi

Publications and source records attributed to M Terzi.

12 recordsLinked to original sources
PubMed1992

A carrot somatic embryo mutant is rescued by chitinase.

At the nonpermissive temperature, somatic embryogenesis of the temperature-sensitive (ts) carrot cell mutant ts11 does not proceed beyond the globular stage. This developmental arrest can be lifted by the addition of proteins secreted by wild-type cells to the culture medium. From this mixture of secreted proteins, a 32-kD glycoprotein, designated extracellular protein 3 (EP3), that allows completion of somatic embryo development in ts11 at the nonpermissive temperature was purified. On the basis of peptide sequences and biochemical characterization, EP3 was identified as a glycosylated acidic endochitinase. The addition of the 32-kD endochitinase to ts11 embryo cultures at the nonpermissive temperature appeared to promote the formation of a correctly formed embryo protoderm. These results imply that a glycosylated acidic endochitinase has an important function in early plant somatic embryo development.

Amino Acid Sequence↗
PubMed1990

A carrot cell variant temperature sensitive for somatic embryogenesis reveals a defect in the glycosylation of extracellular proteins.

The temperature-sensitive carrot cell variant ts11c, arrested in somatic embryogenesis after the globular stage, was characterized. The sensitivity to a shift from 24 degrees C (permissive temperature) to 32 degrees C (non-permissive temperature) is greatest at the globular stage of embryogenesis, while cells proliferating in unorganized fashion and plantlets are not affected. Embryogenesis in ts11c is also arrested at the permissive temperature by replacement of conditioned culture medium with fresh medium. The timing of sensitivity of ts11c to medium replacement coincides with the sensitivity to temperature shift. Both sensitivities are recessive in somatic hybrids between ts11c and wild-type cells. Extracellular glycoproteins synthesized by ts11c at the non-permissive temperature contain much less fucose than those synthesized by the wild type. The glycoproteins synthesized by the variant under non-permissive conditions do not accumulate at the periphery of the embryo, as their wild-type counterparts do, but instead show a diffuse distribution throughout the embryo. The defect in ts11c can be fully complemented by the addition of extracellular wild-type proteins. A revertant of ts11c was isolated that simultaneously reacquired temperature insensitivity and normal glycosylation ability. Collectively, these observations indicate that ts11c is not able to perform proper glycosylation at the non-permissive temperature and suggest that the activity of certain extracellular proteins, essential for the transition of globular to heart stage somatic embryos, depends on the correct modification of their oligosaccharide side-chains.

Biological Transport↗
PubMed1974

Chromosomal variation and the origin of drug-resistant mutants in mammalian cell lines.

Drug-resistant mutants of somatic cell lines fall into two classes: one seems to correspond to classical gene mutation, the other is characterized, albeit transiently, by karyotypic instability, high reversion frequency, and low plating efficiency. An interpretation of the origin of these drug-resistant mutants is offered on the basis of chromosomal variation, which generates variation of the number of copies of each individual chromosome and, consequently, of gene dosage.

Alleles↗