Your evidence comes from museum of the wierd. How about the National Enquirer.
All life on earth is remarkably closely related on a molecular biological scale - as demonstrated by the universal role of DNA, RNA, translation, and the genetic code. Although DNA and proteins could be supposed to be prerequisites for any form of complex organic life, the arbitrary nature of the genetic code suggests that completely independently evolved alien life would have an entirely different code. Hence, alien "genes" might not be compatible with the human protein expression apparatus, in which case cross breeding could not occur.
Furthermore, humans and other organisms are extremely closely related on the genetic scale: for example, humans share between 97% and 99% of their genomic DNA sequence with chimpanzees, and about 30 percent of all human proteins are identical in sequence to the corresponding chimp protein . Phylogenetic comparisons of mitochondrial and ribosomal DNA across species ranging from humans to bacteria verify the evolutionary relationships suggested by the fossil record. Current genetic evidence therefore suggests an intimate genetic relationship between humans and other terrestrial organisms, and provides a strong contrary argument to claims of alien interbreeding.
Here is what they found in 1999:
BOLD Institute, DNA Testing of Ancient Human-like Skull, 1999:
"conclusive evidence that the child was not only human (and male), but both of his parents must have been human as well, for each must have contributed one of the human sex chromosomes"
Further DNA tests were conducted in 2003 by a company called Trace Genetics. They specialise in recovering DNA samples from ancient relics. Below I have copied and pasted their entire report into their DNA testing:
"Report on the DNA analysis from skeletal remains from two skulls
conduced by Trace Genetics
August 12, 2003
Trace Genetics
Two sets of remains were received by Trace Genetics and were processed for genetic
analyses. The remains consisted of two skulls presented by Mr. Lloyd Pye for DNA analysis.
SAMPLING
Prior to attempts to extract DNA from the remains, the remains were inventoried and
taped using a video camera. Video records of the sampling procedure and the initial extraction
on all samples were taken and archived by Trace Genetics.
Samples were cut from the left parietal of an abnormally shaped skull, identified as the
Starchild skull on February 10, 2003. Equipment used to sample was sterilized using a bleach
solution prior to use. Sampling was performed in a room not used for any genetic analyses.
Fragments weighing a total of 0.8g were cut from the parietal using a rotary cutter with a
previously unused blade. The fragments were placed in a sterile conical tube labeled SCS-1 and
stored for analysis. A second 0.7g fragment adjacent to the sample retained by Trace Genetics
was placed in a sterile conical tube labeled SCS-2 and returned to Mr. Pye.
Two teeth were removed from maxilla of a skull presented in association with the
Starchild skull on February 10, 2003. The right first molar tooth and root weighing 1.7g was
removed and labeled “SA-1.” The tooth and root were placed in a sterile conical tube and
retained for genetic analysis by Trace Genetics. A portion of the root was fractured in the
process and remained in the maxilla. The right premolar and root (sample labeled “SA-2”; total
weight 1.0g) were also removed from the maxilla, placed in a sterile conical tube. The SA-2
sample was returned to Mr. Pye.
EXTRACTION AND ANALYSIS OF DNA
SCS-1:
Extraction 1:
A first extraction was performed on a 0.24g fragment of the parietal bone from sample
SCS-1. The extraction was performed in a dedicated ancient DNA laboratory beginning on 7
March 2003 and was performed in parallel to an extraction of SA-1 and a reagent blank (negative
control). Both surfaces of bone were sanded with a rotary sander to remove any surface
contaminants and lacquer preserves present on the outer surfaces of bone. Subsequent to
sanding, the bone was exposed to ultraviolet (UV) irradiation (254nm) for 300 seconds per side.
The bone surface was then cleaned with bleach (2% sodium hypochlorite), rinsed with sterile
EDTA and placed in a fresh 15ml conical tube and immersed in approximately 2ml of 0.5M
EDTA. The tube was sealed with parafilm and placed on a rocker.
After 10 days, the tube was opened and 150μl of 0.1M PTB [1] and 20μl of 100mg/ml
proteinase-K was added to the sample and EDTA. The sample was incubated with agitation
overnight at 64oC. DNA was extracted from the digested sample using a 3-step
phenol/chloroform extraction method. Two extractions with phenol:chloroform:isoamyl
(25:24:1) of equal volume to the digested product were followed by an extraction with an equal
volume of chloroform:isoamyl (24:1). The extracted DNA solution was concentrated by
ammonium-acetate precipitation using two volumes of cold 100% filtered ethanol and 1/2
volume of 5M ammonium acetate. This solution was then stored at -20°C for approximately 4
hours to facilitate precipitation, then centrifuged at high speeds (10,000-12,000rpm) for 15
minutes to pellet the precipitated DNA. The supernatant was discarded and the remaining DNA
pellet dried and resuspended in ~300μl sterile ddH2O. To further purify the DNA and remove
additional PCR inhibitors co-extracted with the DNA, the DNA solution was purified using the
Promegaâ Wizard PCR Preps DNA Purification Kit as directed by the manufacturer. DNA was
eluted from Promegaâ columns with 100μl sterile ddH2O, the elutant labeled SCSex1 and stored
at –20°C.
Attempts to amplify segments of mtDNA from extract SCSex1 were performed as
described below in METHODS. Single amplifications for fragments containing the diagnostic
mutations for Native American haplogroups A, B, C and D[2] did not reveal a known Native
American haplogroup, however, the extraction did not amplify consistently. A single
amplification of a fragment of the mtDNA first hypervariable segment (HVSI) between np
16210 and np 16328 was sequenced using a cycle sequencing procedure with ABI Big-Dye 3.1
chemistry and analyzed on an ABI automated genetic analyzer. The sequence obtained revealed
a transition relative to the Cambridge reference sequence at np16273. This sequence did not
match either any personnel with access to the ancient DNA facilities or a sequence obtained from
Mr. Pye. Subsequent amplifications of this fragment were not successful and the sequence could
not be confirmed. Attempts to amplify fragments of the amelogenin gene located on the X and Y
chromosome[3] were uniformly not successful.
Extraction 2:
A second extraction was performed beginning April 21, 2003 on 0.21g of the parietal
sample from SCS-1. The extraction was performed as above with the following modifications:
1. The sample was run in parallel with a reagent blank (negative control) but was not
processed with any other samples.
2. The bone was exposed to 900 seconds of UV irradiation per side.
3. The bone was completely immersed in 2% sodium hypochlorite for 5 minutes.
4. The sample was left in EDTA with agitation for 22 days prior to digestion with
proteinase-K.
5. At digestion, ~50μl of Tween-20 was added with 100μl of PTB.
6. The silica extraction columns (Promega®) were eluted with 80μl of ddH2O and
sample labeled “SCSe2.”
Attempts to amplify mtDNA for fragments containing the diagnostic mutations for
Native American haplogroups A, B, C and D were performed on extract SCSe2. Multiple
amplifications indicated that the sample possessed an AluI restriction site at np 13262 indicative
of Native American haplogroup C [2]. Sequence obtained for a fragment of the first
hypervariable segment of the mtDNA control region from np16210 to np 16367 revealed
transitions at np16223, np 16298, np 16325 and np 16327. These mutations are characteristic of
haplogroup C in the Americas [4].
Multiple attempts to amplify a segment of the amelogenin gene were unsuccessful using
various amounts of SCSe2 extract as template. 30μl of the original extract was concentrated to a
final volume of ~10μl using a microcon YM-30 concentrator. Attempts to amplify this
concentrated template were not successful.
Extraction 3:
A third extraction was performed beginning on June 4, 2003 as described above for
extraction 2 with the following modifications:
1. The extraction was performed on the entire remaining 0.40g of bone.
2. The sample was immersed in ~3.5ml of EDTA.
3. To ensure adequate demineralization of the sample, the sample was left immersed in
EDTA with agitation for 30 days.
4. The final elution from the silica spin columns (Promega®) was performed twice, each
time with 35μl of ddH2O preheated to 65oC.
Attempts to amplify fragments of mtDNA were performed to test for the presence of
diagnostic mutations fo r Native American haplogroups A and C. The sample did not appear to
possess the diagnostic HaeIII mutation and np663 indicative of haplogroup A. Multiple
amplifications did reveal the presence of the AluI site gain at np13262 indicative of haplogroup C.
A single amplification of a fragment of the amelogenin gene located on the X and Y
chromosomes [3] produced a single amplification product 106bp in length. Multiple subsequent
amplifications did not reproduce this event, as all subsequent attempts did not produce a PCR
product.
SA-1:
Extraction 1:
A first extraction was performed on 0.53g fragment of the molar tooth from sample SA-1
beginning on 7 March 2003 and was performed in parallel to an extraction of SCS-1 (above) and
a reagent blank (negative control). The extraction was performed in the manner describe above
for extraction 1 of SCS-1 save that the outer surface of the tooth, which had previous to sampling
been firmly rooted in the maxilla, was not sanded and the final elution of the silica spin column
(Promega®) was eluted to 100μl and labeled SAex1.
Multiple attempts to amplify segments of mtDNA containing amplifications for
fragments of mtDNA containing the diagnostic mutations for Native American haplogroup A
revealed a HaeIII restriction site at np663 consistent with known Native American haplogroup A
[2]. Amplifications for fragments containing the diagnostic sites for haplogroups B, C and D did
not show presence of mutations indicative of these haplogroups. A single amplification of a
fragment of the mtDNA first hypervariable segment (HVSI) between np 16210 and np 16327
revealed transitions relative to the Cambridge reference sequence at np16223, np16290 and
np16319. These mutations are consistent with Native American haplogroup A.
Multiple amplifications of a fragment of the amelogenin gene on the X and Y
chromosomes consistently produced a single band 106bp in length when visualized on an
electrophoretic gel consistent with DNA from a female [3].
Extraction 2:
A second extraction was performed beginning Ap ril 21, 2003 on 0.42g of the tooth
sample from SA-1. The extraction was performed similar to extraction 1 on SA-1 (above) with
the following modifications:
1. The sample was not run in parallel to any samples from SCS-1.
2. The sample was immersed in EDTA for 26 days prior to digestion with proteinase-K.
The final elution was labeled SAe2 and stored at –20oC.
Multiple amplifications of a mtDNA fragment indicated the presence of a HaeIII
restriction site at np663 indicative of Native American haplogroup A. Amplifications of the
extraction did not possess the AluI site gain at np16262. Multiple amplifications of a fragment of
the amelogenin gene produced a single band when visualized on an electrophoretic gel consistent
with DNA from a female.
The sample taken from the Starchild Skull (SCS-1) has mtDNA consistent with Native
American haplogroup C, as revealed through two independent extractions performed on
fragments of parietal bone. While a single first extraction did not appear to type similarly, this
inconsistent result is likely a product of a low level of contamination. This single extraction
neither amplified consistently nor was the single sequence of HVSI reproducible. Contamination
could have occurred either prior to sampling, introduced in the extraction process, or during PCR
amplifications. It is unlikely that contamination could account for the haplogroup C mtDNA as
this type is not possessed by any researcher with access to the ancient DNA facilities and the
reagent blanks did not indicate systematic contamination in the extractions.
The sample taken from the associated skull (SA-1) has mtDNA consistent with Native
American haplogroup A as determined through both extractions. The sample also appeared be
from a female individual as evidenced by repeated amelogenin typing. It is unlikely that
contamination could account for the haplogroup A mtDNA as this type is not possessed by any
researcher with access to the ancient DNA facilities and the reagent blanks did not indicate
systematic contamination in the extractions.
As mtDNA exists in high copy number (upwards of three orders of magnitude relative to
any single copy nuclear DNA locus), it can be recovered from prehistoric biological material in
sufficient quantities for amplification and analysis using the polymerase chain reaction (PCR)
[see: 7, 8]. MtDNA is present in haploid condition with inheritance being passed down
exclusively through maternal lines [9]. Thus, that the samples analyzed from SCS-1 and SA-1
possessed markedly different mtDNA types excludes a mother-offspring relationship between
the two individuals. As it was possible to type and confirm both to known pre-Columbian
mtDNA types found in the Americas, both individuals most appear to have possessed Native
American mothers.
While it is possible to obtain nuclear DNA as well from ancient samples, the reduced
copy-number at any particular nuclear locus relative to mtDNA makes it less likely that a
particular extract will contain sufficient DNA for the analysis of a nuclear genetic locus using
presently available PCR methods. The ability to amplify nuclear DNA from the SA-1
extractions but not from the SCS-1 extractions could be a product of any of a number of factors.
In ancient DNA analysis, success rates from teeth are generally higher than from bone [10, 11].
Further, there is some indication that X-Ray exposure damages and degrades DNA, which may
have decreased the quantity and quality of DNA available in the bone prior to extraction. The
lone amplification using the amelogenin primers on extract SCSe3 could not be confirmed
through additional amplifications and likely indicates a sporadic contamination of a single PCR
reaction caused either by a female individual in the laboratory or could have been introduced to
laboratory disposables (e.g. pipette tips, PCR reaction tubes). Such contamination has been
noted elsewhere [12] and consequently, any conclusions drawn from the single un-reproduced
PCR reaction should not be taken as any reliable indication as to the DNA present in the sample.
The presence of reliably typed mtDNA from SCS samples does indicate that mtDNA is
present in the bone. The inability to analyze nuclear DNA indicates that such DNA is either not
present or present in sufficiently low copy number to prevent PCR analysis using methods
available at the present time.
Your evidence comes from museum of the wierd. How about the National Enquirer.
