Morphogenesis of the Balbiani body in developing oocytes of an orthopteran, Metrioptera brachyptera , and multiplication of female germline mitochondria

2020 ◽  
Vol 281 (9) ◽  
pp. 1142-1151
Author(s):  
Malgorzata Sekula ◽  
Waclaw Tworzydlo ◽  
Szczepan M. Bilinski
Keyword(s):  
Balbiani Body ◽  
Female Germline

The Balbiani Body in the Female Germline Cells of an Earwig,Opisthocosmia silvestris

2009 ◽  
Vol 26 (11) ◽  
pp. 754-757 ◽  
Author(s):  
Waclaw Tworzydlo ◽  
Malgorzata Kloc ◽  
Szczepan M. Bilinski
Keyword(s):  
Balbiani Body ◽  
Germline Cells ◽  
Female Germline

scholarly journals Selection of mitochondria in female germline cells: is Balbiani body implicated in this process?

2017 ◽  
Vol 34 (11) ◽  
pp. 1405-1412 ◽  
Author(s):  
Szczepan M. Bilinski ◽  
Malgorzata Kloc ◽  
Waclaw Tworzydlo
Keyword(s):  
Balbiani Body ◽  
Germline Cells ◽  
Female Germline ◽  
Selection Of

Inhibition of DMRTA2 impairs human female germline development in xeno-grafted ovaries

2014 ◽  
Author(s):  
Marine Poulain ◽  
Sophie Tourpin ◽  
Vincent Muczynski ◽  
Sebastien Messiaen ◽  
Delphine Moison ◽  
...  
Keyword(s):  
Human Female ◽  
Germline Development ◽  
Female Germline

scholarly journals A hobo Transgene That Encodes the P-Element Transposase in Drosophila melanogaster: Autoregulation and Cytotype Control of Transposase Activity

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 195-204 ◽  
Author(s):  
Michael J Simmons ◽  
Kevin J Haley ◽  
Craig D Grimes ◽  
John D Raymond ◽  
Jarad B Niemi
Keyword(s):  
Drosophila Melanogaster ◽  
Gonadal Dysgenesis ◽  
P Element ◽  
Hsp70 Gene ◽  
Alternate Splicing ◽  
Male And Female ◽  
P Elements ◽  
Male Germline ◽  
Female Germline ◽  
Transposase Expression

Abstract Drosophila were genetically transformed with a hobo transgene that contains a terminally truncated but otherwise complete P element fused to the promoter from the Drosophila hsp70 gene. Insertions of this H(hsp/CP) transgene on either of the major autosomes produced the P transposase in both the male and female germlines, but not in the soma. Heat-shock treatments significantly increased transposase activity in the female germline; in the male germline, these treatments had little effect. The transposase activity of two insertions of the H(hsp/CP) transgene was not significantly greater than their separate activities, and one insertion of this transgene reduced the transposase activity of P(ry+, Δ2-3)99B, a stable P transgene, in the germline as well as in the soma. These observations suggest that, through alternate splicing, the H(hsp/CP) transgene produces a repressor that feeds back negatively to regulate transposase expression or function in both the somatic and germline tissues. The H(hsp/CP) transgenes are able to induce gonadal dysgenesis when the transposase they encode has P-element targets to attack. However, this ability and the ability to induce P-element excisions are repressed by the P cytotype, a chromosomal/cytoplasmic state that regulates P elements in the germline.

scholarly journals Genetic and Molecular Characterization of the Caenorhabditis elegans Gene, mel-26, a Postmeiotic Negative Regulator of MEI-1, a Meiotic-Specific Spindle Component

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 119-128
Author(s):  
M Rhys Dow ◽  
Paul E Mains
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Interactions ◽  
Negative Regulator ◽  
Meiotic Spindle ◽  
Loss Of Function ◽  
Protein Protein Interactions ◽  
Gain Of Function ◽  
Recessive Mutations ◽  
Female Germline

Abstract We have previously described the gene mei-1, which encodes an essential component of the Caenorhabditis elegans meiotic spindle. When ectopically expressed after the completion of meiosis, mei-1 protein disrupts the function of the mitotic cleavage spindles. In this article, we describe the cloning and the further genetic characterization of mel-26, a postmeiotic negative regulator of mei-1. mel-26 was originally identified by a gain-of-function mutation. We have reverted this mutation to a loss-of-function allele, which has recessive phenotypes identical to the dominant defects of its gain-of-function parent. Both the dominant and recessive mutations of mel-26 result in mei-1 protein ectopically localized in mitotic spindles and centrosomes, leading to small and misoriented cleavage spindles. The loss-of-function mutation was used to clone mel-26 by transformation rescue. As suggested by genetic results indicating that mel-26 is required only maternally, mel-26 mRNA was expressed predominantly in the female germline. The gene encodes a protein that includes the BTB motif, which is thought to play a role in protein-protein interactions.

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