abnormal chromatin (abc), a maternal-effect locus in Drosophila melanogaster

1991 ◽  
Vol 98 (2) ◽  
pp. 233-243 ◽  
Author(s):  
K.B. Vessey ◽  
R.L. Ludwiczak ◽  
A.S. Briot ◽  
E.M. Underwood
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Chromosome Structure ◽  
Nuclear Division ◽  
Embryonic Cell ◽  
Female Sterility ◽  
Chromosome 2 ◽  
Maternal Effect Gene ◽  
Embryonic Cell Cycle ◽  
Effect Gene

Mutations in the maternal-effect gene abnormal chromatin (abc) in Drosophila melanogaster result in a variety of defects involving nuclear replication/division. Three recessive alleles of this gene, which maps near 51F on chromosome 2, all result in female sterility. They cause slower embryonic development that is usually abnormal from the earliest nuclear divisions and arrested by the sixth one. Nuclei tend to be large and erratically distributed, some intensely staining. Mitotic asynchrony is common. Few embryos reach the gastrula stage and none hatch. With the weakest allele, fsPL, bridges between nuclei are common; abnormal chromatin clumps that resemble yolk nuclei occur before the other nuclei reach the surface; and spindle anomalies and DNA wads with numerous centrosomes are seen. Females with the stronger alleles, fsA5 and fs27, lay fewer eggs and a smaller proportion of embryos reach blastoderm; developmental arrest occurs earlier, usually with several large nuclei distributed along the length of the embryo. Chorion defects occur in all three mutants. Mitotic asynchrony, nuclear bridging, endoreduplication and nuclear behavior aberrant from the first division suggest that the abc gene product operates in DNA replication/nuclear division. Larval (homozygous F1) neuroblast chromosome structure and mitotic indices are normal, indicating that any mitotic function is strictly maternal, i.e. abc is not a general mitotic gene. Thus abc is one of a few known genes with a maternal effect that appears to function in the embryonic cell cycle.

scholarly journals ON BIOLOGICAL FUNCTIONS MAPPING TO THE HETEROCHROMATIN OF DROSOPHILA MELANOGASTER

Genetics ◽  
1985 ◽  
Vol 109 (4) ◽  
pp. 701-724
Author(s):  
Sergio Pimpinelli ◽  
William Sullivan ◽  
Mary Prout ◽  
L Sandler
Keyword(s):  
Maternal Effect ◽  
Autosomal Recessive ◽  
Early Time ◽  
Drosophila Embryo ◽  
Chromosome 2 ◽  
Normal Allele ◽  
Hoechst 33258 ◽  
Maternal Effect Gene ◽  
Drosophila Heterochromatin ◽  
Effect Gene

ABSTRACT We examined the behavior of an autosomal recessive maternal-effect mutation, abnormal-oocyte (abo), that is located in the euchromatin of the left arm of chromosome 2. When homozygous in females, abo results in a marked reduction in the probability that an egg produced by a mutant mother will develop into an adult. However, this probability is increased if the fertilizing sperm delivers to the egg either a normal allele of the maternal-effect gene or a specific type of heterochromatin (called ABO) that is located in small regions of the X and Y chromosome constitutive heterochromatin as well as in some autosomal heterochromatin. These regions, moreover, all react to Hoechst 33258 fluorescent dye identically and specifically. The amelioration of the maternal effect produced by this heterochromatin differs temporally from that caused by the normal allele of the euchromatic gene: the heterochromatin reduces only precellular blastoderm mortality, whereas the normal allele of the euchromatic gene reduces only postblastoderm mortality. Thus, although the genome of the preblastoderm Drosophila embryo is apparently mostly silent, the ABO-containing heterochromatin functions at this early time. Finally, preliminary data indicate that abo is but one member of a cluster of linked genes, each of which interacts with its own normal allele and with a different, locus-specific, heterochromatic factor. From these observations, it appears that Drosophila heterochromatin contains developmentally important genetic elements, and that a functional concomitant of heterochromatic location is gene action at a developmental stage during which the activity of the euchromatic genome is as yet undetectable. Some general implications of these inferences are considered.

scholarly journals foxr1is a novel maternal-effect gene in fish that regulates embryonic cell growth viap21andrictor

2018 ◽  
Author(s):  
Caroline T. Cheung ◽  
Amélie Patinote ◽  
Yann Guiguen ◽  
Julien Bobe
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Maternal Effect ◽  
Early Stage ◽  
Growth Arrest ◽  
Embryonic Cell ◽  
Female Reproduction ◽  
Specific Expression ◽  
Maternal Effect Gene ◽  
Effect Gene

AbstractThe family of forkhead box (Fox) transcription factors regulate gonadogenesis and embryogenesis, but the role offoxr1/foxn5in reproduction is unknown. Evolution offoxr1in vertebrates was examined and the gene found to exist in most vertebrates, including mammals, ray-finned fish, amphibians, and sauropsids. By quantitative PCR and RNA-seq, we found thatfoxr1had an ovarian-specific expression in zebrafish, a common feature of maternal-effect genes. In addition, it was demonstrated usingin situhybridization thatfoxr1was a maternally-inherited transcript that was highly expressed even in early-stage oocytes and accumulated in the developing eggs during oogenesis. We also analyzed the function offoxr1in female reproduction using a zebrafish CRISPR/Cas9 knockout model. It was observed that embryos from thefoxr1-deficient females had a significantly lower survival rate whereby they either failed to undergo cell division or underwent abnormal division that culminated in growth arrest at around the mid-blastula transition and early death. These mutant-derived eggs contained a dramatically increased level ofp21, a cell cycle inhibitor, and reducedrictor, a component of mTOR and regulator of cell survival, which were in line with the observed growth arrest phenotype. Our study shows for the first time thatfoxr1is an essential maternal-effect gene and is required for proper cell division and survival via the p21 and mTOR pathways. These novel findings will broaden our knowledge on the functions of specific maternal factors stored in the developing egg and the underlying mechanisms that contribute to reproductive fitness.Summary sentenceThefoxr1gene in zebrafish is a novel maternal-effect gene that is required for proper cell division in the earliest stage of embryonic development possibly as a transcriptional factor for cell cycle progression regulators,p21andrictor.

scholarly journals DOSAGE OF THE MATERNAL EFFECT GENE ASSOCIATED WITH THE TUMOROUS-HEAD ABNORMALITY IN DROSOPHILA MELANOGASTER

Genetics ◽  
1972 ◽  
Vol 72 (2) ◽  
pp. 377-380
Author(s):  
R M Siervogel
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Product ◽  
Maternal Effect ◽  
Specific Gene ◽  
Maternal Effect Gene ◽  
Effect Gene

ABSTRACT The penetrance of tuh-3 observed in the progeny of triploids with two doses of tuh-1 was not statistically different from that occurring in the progeny of their diploid sisters with two doses. A higher penetrance was observed in the progeny of triploids with three doses of tuh-1 than in the progeny of their diploid sisters with two doses. These observations suggest that the maternal effect responsible for increasing the penetrance of tuh-3, the gene causing the tumorous-head abnormality, is caused by a specific gene product of tuh-1, the maternal-effect allele. In addition there is probably a maternal-effect threshold, lying between amounts produced by one and two doses of tuh-1, below which no increased penetrance of tuh-3 is observed.

scholarly journals A NOTE ON THE MATERNAL EFFECT MUTANTS DAUGHTERLESS AND ABNORMAL OOCYTE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler
Keyword(s):  
Drosophila Melanogaster ◽  
Maternal Effect ◽  
Sex Chromosome ◽  
Chromosome 2 ◽  
Dominant Marker ◽  
Enhancing Effect ◽  
X Irradiation ◽  
The Right ◽  
Chromosome Breakpoint ◽  
Special Region

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.

scholarly journals Maternal-effect gene Ces5/Ooep/Moep19/Floped is essential for oocyte cytoplasmic lattice formation and embryonic development at the maternal-zygotic stage transition

2010 ◽  
Vol 15 (8) ◽  
pp. 813-828 ◽  
Author(s):  
Fumi Tashiro ◽  
Masami Kanai-Azuma ◽  
Satsuki Miyazaki ◽  
Masahiro Kato ◽  
Tomofumi Tanaka ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Maternal Effect ◽  
Maternal Effect Gene ◽  
Stage Transition ◽  
Lattice Formation ◽  
Effect Gene
Sign in / Sign up

Export Citation Format

Share Document