Meiotic Drivers: Suppressors and Distorters in Drosophila
While rare, meiotic drive can be observed in Drosophila and is usually marked by sex-ratio distortion. This study takes a closer look at molecular mechanisms of the distorters MDox and Dox and the suppressors tmy and nmy.
icon search Searchable Transcript
Toggle between list and paragraph view.
[00:00:01.980]Hi, my name is Peyton Alder,
[00:00:03.450]and I am excited to present to you my
research today, over my meiotic drivers,
[00:00:07.380]suppressors and distorters
[00:00:10.170]So a little bit of
background into my research.
[00:00:12.480]My research has focused around the
principle of Mendelian segregation.
[00:00:17.130]So this states that an allele pair segregate
during gamete formation and will randomly
[00:00:21.450]combine at fertilization.
[00:00:23.400]This is very important in creating
genetic variability in order to help a
[00:00:27.810]population combat the negative
effects of natural selection,
[00:00:31.500]and also in producing the 50:50 sex
ratio that we observe in nature.
[00:00:36.720]So my research has focused
around when this does not occur.
[00:00:41.280]So non-mendelian segregation,
[00:00:43.620]this is also known as meiotic drive
and normally will cause a sex ratio
[00:00:49.440]The two disorters that I've been focusing
on specifically are MDox and Dox.
[00:00:54.420]So MDox is called mother of
dox and Dox is distorter on X.
[00:00:59.850]These are X-linked genes and
[00:01:03.660]And they work to cause the
disruption of Y bearing sperm,
[00:01:07.140]which causes males to produce
bias progeny sex ratios.
[00:01:11.100]So we normally don't see this in nature
as they are suppressed by Nmy and
[00:01:17.010]So Nmy stands for not much yang
and tmy stands for too much yin
[00:01:22.080]these both work to suppress these
Dox and Mdox distorters by producing
[00:01:26.520]non-coding RNA molecules
that will instigate the
destruction of Dox and MDox
[00:01:32.520]We have found that double mutant males
carrying non-functional alleles at both
[00:01:36.630]the Dox and nmy locuses exhibit
normal sex ratios and spermatogenesis.
[00:01:41.880]So this has led to the inference that
these disorters and suppressors are
[00:01:45.360]connected and that the primary
function of these Dox,
[00:01:48.510]alleles is to cause the
[00:01:53.690]Our purpose of our experiment was to
determine the relationship between Nmy,
[00:01:57.830]Tmy, MDox and Dox,
[00:01:59.660]and more specifically how these disorders
are influencing the sex ratios in
[00:02:03.890]Drosophila simulans and how these
are prevented by these suppressors.
[00:02:08.660]We had hypothesized that the absence of
Tmy or Nmy allows for unregulated
[00:02:12.770]Dox and MDox to attack
the Y bearing sperm,
[00:02:15.950]ultimately causing an excess
of daughters in these offspring
[00:02:22.160]There were two main experiments set up.
[00:02:24.110]So previously we had put several
wild-type Drosophila simulans
[00:02:29.060]X chromosomes. We had taken these
and put them in fertility tests.
[00:02:33.290]So we took males who had,
[00:02:36.590]who possessed all these types of X
chromosomes and are also homozygous for
[00:02:41.330]Mutant alleles at Nmy and Tmy,
[00:02:43.400]and put them with three females
and the offspring of this cross is
[00:02:48.080]phenotypes number and sex
were all recorded
[00:02:52.520]in order to determine
the phenotypes of these,
[00:02:55.370]of these offspring the flies are
looked at under special lighting.
[00:02:58.850]So Nmy mutants are tagged with
DS red or red fluorescent protein,
[00:03:02.590]as it is also called and will
exhibit a Glint in the eye.
[00:03:06.580]And Tmy mutanst are tagged
with green fluorescent protein.
[00:03:09.880]And so will glow in the dark when
looked at under a special lighting.
[00:03:15.010]Our second round of experiments involve
the same wild-type X chromosomes that we
[00:03:19.870]use in the first part. Instead of
the males possessing these though,
[00:03:24.820]females with these wild type X
chromosomes were crossed with
[00:03:29.530]Drosophila mauritiana males.
[00:03:33.430]So this gave the offspring a
Y chromosome from Drosophila mauritiana,
[00:03:37.990]which is a different species of Drosophila and both the females and the
[00:03:42.880]males had homozygous mutant alleles at
tmy and nmy on the third chromosome.
[00:03:49.420]The males resulting from this cross were
then also put into fertility tests,
[00:03:53.560]similar to the ones used above.
[00:03:55.570]So one of these males was
put with three females.
[00:03:59.320]These males ranged in phenotypes from
just having mutant alleles at tmy and
[00:04:03.670]tmy from just having the mutant alleles at
Nmy and those who had mutant alleles
[00:04:08.560]at both. And again, the offsprings
phenotypes number and sex were recorded.
[00:04:15.840]Lastly, I am currently testing
primers in order to genotype,
[00:04:21.390]so they're still in the stage
of being standardized.
[00:04:23.910]so they produce a single
band that we want.
[00:04:27.060]So that will be a next step
in the experiment. Okay.
[00:04:31.620]Moving on to the data and
results from these experiments.
[00:04:34.350]So the results of the first fertility
tests we performed with the Drosophila
[00:04:38.250]simulans on wild-type X chromosomes who
had the regular Y chromosome also from
[00:04:43.140]simulans. These were all
found to be varying and different.
[00:04:46.800]So we found fertility phenotypes
ranging from total sterility to
[00:04:51.660]fertility, to a sex ratio exhibited.
[00:04:54.630]these results can be observed
in figure two down below.
[00:04:58.740]So we also see that which loci
they were mutant that
[00:05:03.720]also had an effect.
[00:05:05.310]So some more sterile when they
were mutant and only nmy and
[00:05:10.050]nmy and some were fertile.
[00:05:12.300]Then when they had to meet when
they were muting at tmy and tmy.
[00:05:16.200]So we are seeing a range of varying
phenotypes for these offspring.
[00:05:23.400]When we looked at the results
of the fertility tests,
[00:05:26.970]which contain the mauritiana Y chromosome,
[00:05:30.450]we saw a similar range or similar
setup of these fertility
[00:05:34.980]phenotypes. So we also saw
a range there. However,
[00:05:38.040]the sex ratio distortion was a lot
less prominent than when it was just
[00:05:42.930]with the regular Y chromosome
for Drosophila simulans.
[00:05:46.980]And we also saw that temperature had
a slight effect on these as well.
[00:05:50.610]So it seemed that some were more
sensitive to temperature changes than
[00:05:55.560]others. So when
interpreting these results,
[00:06:00.430]we can conclude that each X chromosome
is affected differently by the distorters
[00:06:05.200]and suppressors. And so we were wanting
to understand these mechanisms more.
[00:06:11.020]We can also infer that these distorters
are targeting the Y chromosome as we were
[00:06:14.920]seeing an excess of daughters.
[00:06:16.180]So it is most likely attacking these
Y chromosomes and not allowing them
[00:06:21.160]to be passed on to the next generation.
[00:06:23.920]So that's why we were seeing more
daughters as daughters inherit two Xs and
[00:06:28.480]males that inherit X, Y.
[00:06:33.130]And lastly, from these fertility tests,
[00:06:34.780]we can also assume that the Y mauritiana
chromosome is more resistant than the
[00:06:39.700]Y simulans. And we're
not sure why this is yet,
[00:06:43.480]but it is interesting to know,
[00:06:45.250]as we see that the sex ratio is closer
to what we observe in nature with that 50
[00:06:49.750]50 that we want compared to the
Y chromosome for the simulans.
[00:06:55.270]So some future directions we can
take with this is we are currently,
[00:06:59.110]as I said before, we are currently
using primers to start
[00:07:01.760]genotyping these and see exactly
what sequences and what
is different between these
[00:07:05.860]chromosomes that can hopefully tell
us why some are more resistant,
[00:07:09.760]why some are sterile and why some are
fertile when you get these alleles.
[00:07:14.650]And also we would like
to look at, ago2,
[00:07:18.700]so this is a gene that
is required for tmy,
[00:07:22.270]and nmy to be able to
suppress these distorters.
[00:07:24.460]So we just want to look further
into this to see if there's any
[00:07:29.110]underlying mechanisms here that can also
help us understand how these distorters
[00:07:32.920]and suppressors work
[00:07:36.160]I would like to thank the Meiklejohn
lab for their guidance, knowledge, time,
[00:07:40.030]And I would also like to thank
UCARE for the opportunity to pursue this
[00:07:44.590]I hope to continue this in the future
and to slowly learn more about the
[00:07:48.400]mechanisms that involve these
distorters and suppressors.
[00:07:52.540]Thank you so much for your time.
[00:07:53.950]And I look forward to hearing
your comments and questions.
Log in to post comments