Null alleles reveal novel requirements for Bic-D during Drosophila oogenesis and zygotic development

Development ◽  
1994 ◽  
Vol 120 (5) ◽  
pp. 1233-1242 ◽  
Author(s):  
B. Ran ◽  
R. Bopp ◽  
B. Suter
Keyword(s):  
Germ Line ◽  
Null Alleles ◽  
Cell Fates ◽  
New Class ◽  
Specific Accumulation ◽  
Normal Polarity ◽  
Female Germ Line ◽  
Low Levels ◽  
Drosophila Ovary ◽  
Sister Cells

In the Drosophila ovary, the Bicaudal-D (Bic-D) gene is required for the differentiation of one of 16 interconnected cystocyte sister cells into an oocyte. A new class of Bic-Dnull alleles reveals a novel requirement for Bic-D for zygotic viability. In the germ line, the null mutations show that developmental processes that take place in germarial region 1, even those that create asymmetry, are independent of Bic-D function. Bic-D is then required to establish oocyte identity in one cystocyte and is essential, not only for the oocyte-specific accumulation of all oocyte markers that we have tested so far, but also for the posterior migration of the oocyte. In addition, normal polarity amongst the nurse cells requires Bic-D, indicating that the creation of different nurse cell identities may depend on oocyte determination. Our results show that different processes in early oogenesis require different amounts of Bic-D in a process-specific way and certain later processes can proceed at low levels of Bic-D. This suggests that the patterning of the female germ line and the development of an oocyte depend on differential responses to a single activity that is capable of initiating distinct oogenesis processes and can establish different cell fates.

scholarly journals BCL2-modifying factor promotes germ cell loss during murine oogenesis

Reproduction ◽  
2016 ◽  
Vol 151 (5) ◽  
pp. 553-562 ◽  
Author(s):  
Kavitha Vaithiyanathan ◽  
Seng H Liew ◽  
Nadeen Zerafa ◽  
Thilini Gamage ◽  
Michele Cook ◽  
...  
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Germ Line ◽  
Cell Loss ◽  
Regulatory Proteins ◽  
Primordial Follicles ◽  
Large Numbers ◽  
Female Germ Line ◽  
Low Levels

Abstract Apoptosis plays a prominent role during ovarian development by eliminating large numbers of germ cells from the female germ line. However, the precise mechanisms and regulatory proteins involved in germ cell death are yet to be determined. In this study, we characterised the role of the pro-apoptotic BH3-only protein, BCL2-modifying factor (BMF), in germ cell apoptosis in embryonic and neonatal mouse ovaries. BMF protein was immunohistochemically localised to germ cells at embryonic days 15.5 (E15.5) and E17.5 and postnatal day 1 (PN1), coincident with entry into the meiotic prophase, but was undetectable at E13.5, and only present at low levels at PN3 and PN5. Consistent with this expression pattern, loss of BMF in female mice was associated with a decrease in apoptosis at E15.5 and E17.5. Furthermore, increased numbers of germ cells were found in ovaries from Bmf−/− mice compared with WT animals at E15.5 and PN1. However, germ cell numbers were comparable between Bmf−/− and WT ovaries at PN3, PN5 and PN10. Collectively, these data indicate that BMF mediates foetal oocyte loss and its action limits the maximal number of germ cells attained in the developing ovary, but does not influence the number of primordial follicles initially established in ovarian reserve.

pitkinD, a Novel Gain-of-Function Enhancer of Position-Effect Variegation, Affects Chromatin Regulation During Oogenesis and Early Embryogenesis in Drosophila

Genetics ◽  
2001 ◽  
Vol 157 (3) ◽  
pp. 1227-1244 ◽  
Author(s):  
Steffi Kuhfittig ◽  
János Szabad ◽  
Gunnar Schotta ◽  
Jan Hoffmann ◽  
Endre Máthé ◽  
...  
Keyword(s):  
Germ Line ◽  
Position Effect ◽  
Early Embryogenesis ◽  
Position Effect Variegation ◽  
Chromatin Regulation ◽  
Gain Of Function ◽  
Position Effects ◽  
Dominant Female ◽  
Effect Variegation ◽  
Female Germ Line

Abstract The vast majority of the >100 modifier genes of position-effect variegation (PEV) in Drosophila have been identified genetically as haplo-insufficient loci. Here, we describe pitkinDominant (ptnD), a gain-of-function enhancer mutation of PEV. Its exceptionally strong enhancer effect is evident as elevated spreading of heterochromatin-induced gene silencing along euchromatic regions in variegating rearrangements. The ptnD mutation causes ectopic binding of the SU(VAR)3-9 heterochromatin protein at many euchromatic sites and, unlike other modifiers of PEV, it also affects stable position effects. Specifically, it induces silencing of white+ transgenes inserted at a wide variety of euchromatic sites. ptnD is associated with dominant female sterility. +/+ embryos produced by ptnD/+ females mated with wild-type males die at the end of embryogenesis, whereas the ptnD/+ sibling embryos arrest development at cleavage cycle 1-3, due to a combined effect of maternally provided mutant product and an early zygotic lethal effect of ptnD. This is the earliest zygotic effect of a mutation so far reported in Drosophila. Germ-line mosaics show that ptn+ function is required for normal development in the female germ line. These results, together with effects on PEV and white+ transgenes, are consistent with the hypothesis that the ptn gene plays an important role in chromatin regulation during development of the female germ line and in early embryogenesis.

Dedicated protection for the female germ line

2006 ◽  
Vol 8 (1) ◽  
pp. 8-8
Author(s):  
Magdalena Skipper
Keyword(s):  
Germ Line ◽  
Female Germ Line

Multiple products from the shavenbaby-ovo gene region of Drosophila melanogaster: relationship to genetic complexity

1994 ◽  
Vol 14 (10) ◽  
pp. 6809-6818
Author(s):  
M D Garfinkel ◽  
J Wang ◽  
Y Liang ◽  
A P Mahowald
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Line ◽  
Gene Region ◽  
Multiple Products ◽  
Zinc Finger Motifs ◽  
Genetic Complexity ◽  
Complex Locus ◽  
Female Germ Line ◽  
Sensory Structures ◽  
Pole Cells

The Drosophila melanogaster shavenbaby (svb)-ovo gene region is a complex locus, containing two distinct but comutable genetic functions. ovo is required for survival and differentiation of female germ line cells and plays a role in germ line sex determination. In contrast, svb is required in both male and female embryos for the production of epidermal locomotor and sensory structures. Sequences required for the two genetic functions are partially overlapping. ovo corresponds to a previously described germ line-dependent 5.0-kb poly(A)+ mRNA that first appears in the germarium and accumulates in nurse cells during oogenesis. The 5.0-kb mRNA is stored in the egg, but it is rapidly lost in the embryos except for its continued presence in the germ line precursor pole cells. The ovo mRNA predicts a 1,028-amino-acid 110.6-kDa protein homologous with transcription factors. We have identified an embryonic mRNA, 7.1 kb in length, that contains exons partially overlapping those of the 5.0-kb poly(A)+ mRNA. The spatial distribution of this newly discovered transcript during midembryogenesis suggests that it corresponds to the svb function. The arrangement of exons common to the 5.0- and 7.1-kb mRNAs suggests that the Ovo and Svb proteins share DNA-binding specificity conferred by four Cys2-His2 zinc finger motifs but differ functionally in their capacity to interact with other components of the transcription machinery.

scholarly journals Genetic structure and dispersal patterns of the invasive psocid Liposcelis decolor (Pearman) in Australian grain storage systems

2010 ◽  
Vol 100 (5) ◽  
pp. 521-527 ◽  
Author(s):  
K.M. Mikac ◽  
N.N. FitzSimmons
Keyword(s):  
Genetic Structure ◽  
Isolation By Distance ◽  
Geographic Distance ◽  
Allelic Diversity ◽  
Mantel Test ◽  
Null Alleles ◽  
Dispersal Patterns ◽  
Long Distance ◽  
Population Comparisons ◽  
Low Levels

AbstractMicrosatellite markers were used to investigate the genetic structure among invasive L. decolor populations from Australia and a single international population from Kansas, USA to determine patterns of dispersal. Six variable microsatellites displayed an average of 2.5–4.2 alleles per locus per population. Observed (HO) heterozygosity ranged from 0.12–0.65 per locus within populations; but, in 13 of 36 tests, HO was less than expected. Despite low levels of allelic diversity, genetic structure estimated as θ was significant for all pairwise comparisons between populations (θ=0.05–0.23). Due to suspected null alleles at four loci, ENA (excluding null alleles) corrected FST estimates were calculated overall and for pairwise population comparisons. The ENA-corrected FST values (0.02–0.10) revealed significant overall genetic structure, but none of the pairwise values were significantly different from zero. A Mantel test of isolation by distance indicated no relationship between genetic structure and geographic distance among all populations (r2=0.12, P=0.18) and for Australian populations only (r2=0.19, P=0.44), suggesting that IBD does not describe the pattern of gene flow among populations. This study supports a hypothesis of long distance dispersal by L. decolor at moderate to potentially high levels.

scholarly journals GENETIC ANALYSIS OF THREE DOMINANT FEMALE-STERILE MUTATIONS LOCATED ON THE X CHROMOSOME OF DROSOPHILA MELANOGASTER

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 309-325
Author(s):  
D Busson ◽  
M Gans ◽  
K Komitopoulou ◽  
M Masson
Keyword(s):  
X Chromosome ◽  
Germ Line ◽  
Female Sterility ◽  
Recessive Mutation ◽  
Wild Type Allele ◽  
Wild Type ◽  
Allelic Series ◽  
Type Allele ◽  
Dominant Female ◽  
Female Germ Line

ABSTRACT Three dominant female-sterile mutations were isolated following ethyl methanesulfonate (EMS) mutagenesis. Females heterozygous for two of these mutations show atrophy of the ovaries and produce no eggs (ovoD  1) or few eggs (ovoD  2); females heterozygous for the third mutation, ovoD  3, lay flaccid eggs. All three mutations are germ line-dependent and map to the cytological region 4D-E on the X chromosome; they represent a single allelic series. Two doses of the wild-type allele restore fertility to females carrying ovoD  3 and ovoD  2, but females carrying ovoD  1 and three doses of the wild-type allele remain sterile. The three mutations are stable in males but are capable of reversion in females; reversion of the dominant mutations is accompanied by the appearance, in the same region, of a recessive mutation causing female sterility. We discuss the utility of these mutations as markers of clones induced in the female germ line by mitotic recombination as well as the nature of the mutations.

scholarly journals Increased Expression of Maturation Promoting Factor Components Speeds Up Meiosis in Oocytes from Aged Females

2018 ◽  
Vol 19 (9) ◽  
pp. 2841 ◽  
Author(s):  
Marketa Koncicka ◽  
Anna Tetkova ◽  
Denisa Jansova ◽  
Edgar Del Llano ◽  
Lenka Gahurova ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Maternal Age ◽  
Germ Line ◽  
Nuclear Lamina ◽  
Nuclear Envelope Breakdown ◽  
Meiotic Progression ◽  
Translational Activity ◽  
Female Germ Line ◽  
Mammalian Female ◽  
Meiosis I

The rate of chromosome segregation errors that emerge during meiosis I in the mammalian female germ line are known to increase with maternal age; however, little is known about the underlying molecular mechanism. The objective of this study was to analyze meiotic progression of mouse oocytes in relation to maternal age. Using the mouse as a model system, we analyzed the timing of nuclear envelope breakdown and the morphology of the nuclear lamina of oocytes obtained from young (2 months old) and aged females (12 months old). Oocytes obtained from older females display a significantly faster progression through meiosis I compared to the ones obtained from younger females. Furthermore, in oocytes from aged females, lamin A/C structures exhibit rapid phosphorylation and dissociation. Additionally, we also found an increased abundance of MPF components and increased translation of factors controlling translational activity in the oocytes of aged females. In conclusion, the elevated MPF activity observed in aged female oocytes affects precocious meiotic processes that can multifactorially contribute to chromosomal errors in meiosis I.

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