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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
ΔHisC, Df(2L)HisCED1429
Sequence coordinates
2L:21,400,839..21,400,839 (Df(2L)His[C]:bk1)
2L:21,573,418..21,573,418 (Df(2L)His[C]:bk2)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data
Genetic mapping information

Scer\FRT-mediated recombination between the two progenitor insertions has resulted in the deletion of the genomic sequence between them. This deletion removes the entire histone complex.

Comments on Cytology
Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Partially deleted / disrupted
Molecular Data
Partially deleted
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
Molecular Data
Affected Genes Inferred by Location
Phenotypic Data
In combination with other aberrations
NOT in combination with other aberrations

Df(2L)HisC homozygotes are embryonic lethal, as they cannot progress past the S phase of 15th cycle.

Df(2L)HisC homozygotes are unable to complete the cell cycle and die as embryos.

Df(2L)HisC homozygous mutant animals that are derived from heterozygous parents contain only maternal histone mRNA and proteins, which are sufficient to complete the first 14 cell division cycles of the embryo.

Chromatin from Df(2L)HisC mutant embryos is more accessible to MNase than control chromatin, leading to a more rapid generation of mononucleosomal DNA fragments and a decrease in nucleosome occupancy.

Most cells from Df(2L)HisC mutant embryos enter S-phase in cycle 15 before mitosis, but the spatil pattern of replicating cells is different from the highly stereotyped wild-type pattern.

The absence of de novo histone supply in Df(2L)HisC embryos reduces the rate of DNA synthesis shortly after the initiation of DNA replication, resulting in an extended S phase in mutant cells.

The ATM/Chk2 checkpoint mechanism is still function in Df(2L)HisC mutants.

Nucleosome density is affected in Df(2L)HisC mutant cells.

Homozygotes die during embryogenesis. The embryos complete the first 14 cycles of embryogenesis with no scorable defects and undergo mitosis 14 similarly to wild type. However, the embryos do not undergo mitosis 15.

Increasing copy numbers of the histone gene repeat unit provided by transgenic constructs can rescue the Df(2L)HisC phenotype: Df(2L)HisC homozygotes that are also homozygous for M{1xHisGU.wt} develop a defective cuticle (Df(2L)HisC homozygotes do not develop a cuticle). Df(2L)HisC homozygotes that are also homozygous for M{3xHisGU.wt} develop a wild-type cuticle pattern but fail to hatch. Df(2L)HisC homozygotes that carry four copies of M{3xHisGU.wt} (homozygous for two different insertions of M{3xHisGU.wt}) are rescued to become fertile adults with no visible morphological defects.

Stocks (0)
Notes on Origin
Balancer / Genotype Variants of the Aberration
Separable Components
Other Comments
Synonyms and Secondary IDs (5)
References (11)