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Poster Full Abstracts - Gametogenesis and Organogenesis
Poster board number is above title. The first author is the presenter
286
morphogenesis.
578B
Jak-STAT regulation of Drosophila germ cell sex determination.
Matthew J. Wawersik, Andrea Lin, Tigist Tamir, Rebecca Obniski. Biology Dept, Col
William & Mary, Williamsburg, VA.
Germ cells are the only cells in the body that make sperm and eggs required for sexual reproduction. Proper germ cell development is, therefore, essential
for survival of future generations. A critical step in this process is the decision made by germ cells to develop along male or female fates. In flies and mice,
both cell autonomous and somatic signals control germline sexual identity. We have previously shown that Jak-STAT activation in Drosophila germ cells by
male somatic gonad plays a critical role in establishment of male germ cell fate during embryogenesis (Wawersik et al, 2005). However, the extent to which
this pathway promotes germ cell sex determination is not clear. Here, we show that hyperactivation of the Jak-STAT pathway during ovary development is
sufficient to induce male germline gene expression in adult XX germ cells. Induction of these genes correlates both spatially and temporally with formation
of germ cell tumors that fail to develop into functional sperm or eggs, a hallmark of altered germ cell sex determination. We also find that XX germ cells
masculinized by mutations in snf and ovo induce STAT gene expression in a subset of ovarian germ cell tumors. Finally, we show that genetic interactions
between snf and jak result in ovarian germ cell tumor formation. Together, these data suggests that the Jak-STAT pathway plays a direct role in germ cell
sex determination and maintenance of sexual identity, and that there is significant cross talk between the pathways that control male vs. female germline
development.
579C
microRNA miR-7 targets Tramtrack69 to regulate a developmental switch in Drosophila follicle cells.
Yi-Chun Huang, Laila Smith, John Poulton,
Wu-Min Deng. Dept Biological Sci, Florida State Univ, Tallahassee, FL.
Development in multicellular organisms consist both small incremental changes and major switches of cell differentiation and proliferation status. During
Drosophila oogenesis, the follicular epithelial cells undergo two major developmental switches with global changes in the cell cycle program. One such
switch, the switch from the endoreplication cycles to a gene amplification phase, during which special genomic regions undergo repeated site-specific
replication, is attributed to Notch downregulation, Ecdysone signaling activation and upregulation of zinc finger protein Tramtrack69 (Ttk69) in follicle
cells. Here we report that microRNA miR-7 exerts an additional layer of regulation in this developmental switch through targeting Ttk69 transcripts. miR-7
targets the 3’ UTR of ttk69 transcripts and regulates Ttk69 expression in a dose dependent manner. Overexpression of miR-7 effectively blocks the switch
from the endocycle to gene amplification through its regulation on ttk69. miR-7 also coordinates other cell differentiation events that lead to the formation of
the mature egg. Our studies reveal the important role miR-7 plays in coordinating developmental switches in association with signal transduction pathways.
580A
Genetic Probing of Drosophila glycine requirements.
Christopher W. Bazinet, Ujwala Gosavi, Debaki Sarkar. Dept Biological Sci, Saint John's Univ,
Queens, NY.
Recent work from a number of laboratories has revealed that a posttranslational modification of microtubules via glycylation, the addition of glycine
residues to one or more aspartate residues near the C-terminus of tubulin subunits, may be critical for regulating the stability and motility of microtubule-
based structures. The extensive glycylation of axonemal microtubules in Drosophila's extraordinarily long sperm implies a significant requirement for
glycine within the spermatogenic cyst. Observations from our laboratory indicate that the gene product of Neurotransmitter transporter-like (Ntl), expressed
and required only in the testis, functions as a glycine transporter for supplementing the glycine stores in spermatogenic cysts. In its absence, glycylation
levels of testis tubulin is reduced, and sperm fail to be transferred from the testis into the seminal vesicle. Thus, manipulation of glycine levels within the
testis may offer a means for regulating male fertility in insects. As a first step towards manipulating glycine metabolism in Drosophila, we have mobilized a
P element insertion at the 5’ end of CG3011, encoding serine-glycine hydroxymethyl transferase (SGHM). Removal of the hydroxymethyl group from serine
by SGHM is the primary or only means by which cells produce glycine. Mutations comprising two lethal complementation groups, one of which presumable
represents the SGHM gene, have been recovered after this transposon mutagenesis. However, supplementation of Drosophila food with glycine fails to
rescue mutants from either complementation group. This indicates that although glycine is not an essential amino acid, neither can it be provided to SGHM[-
] cells in the diet. Instead, glycine synthesis appears to be cell autonomous.
581B
tut
coordinates proliferation and differentiation of spermatogonia in Drosophila.
Di Chen
1,2
, Bangxia Suo
1
, Shaowei Zhao
1,2
, Qing Geng
1,2
, Yu Gao
1,2
,
Zhaohui Wang
1
. 1) Institute of Genetics and Developmental Biology, Beijing; 2) Graduate University of Chinese Academy of Sciences.
Drosophila spermatogenesis represents an excellent model system to study how proliferation and differentiation are coordinated. In order to identify more
factors involved in this process, we conducted a large-scale EMS screen, through which we obtained an interesting mutant, homozygous viable but
containing tiny testes full of un-differentiated germ cells. We mapped this mutation to a novel gene predicted to encode an RNA binding protein and
designated this new gene as
tumorous testis
(
tut
). The over-proliferating germ cells in
tut
mutant testis are spermatogonia, the mitotic amplifying germ cells.
Further analyses indicate that
tut
represents an intrinsic factor for regulating spermatogonial proliferation. We tried genetic interaction tests and found that
tut
and
bam
interact with each other to coordinate proliferation and differentiation of spermatogonia. We also found that Tut protein is strictly regulated and
JAK-STAT signaling from somatic cells inhibits
tut
function in germline stem cells. Currently, we are studying the molecular mechanism by which
tut
coordinates spermatogonial proliferation and differentiation.
582C
Screening for dominant enhancers of Segregation distortion.
Kaylie Church, Janna McLean. Olivet Nazarene University, Bourbonnais, IL.
Segregation distortion is a meiotic drive system that results in the favorable inheritance of the
SD
chromosome over the
SD
+
counterpart. It is understood
that
SD
produces a malfunctioning form of RanGAP; instead of being able to move in and out of the nucleus this truncated RanGAP is unable to be exported
and therefore aggregates within the nucleus. This appears to affect
Rsp
s
during the condensation phase of spermatogenesis; the exact mechanism for this is