If mutations can go viral, adaptationism is less annoying.

Feb. 9, 2016: I have edited the paragraph beginning with "Exciting..." to remove details of mutation rates because my initial posting was probably wrong about coding vs. non-coding mutation rates. To fix that requires much more nuance than is relevant for the point I'm making in that paragraph, not to mention much more nuance than I'm capable of grasping immediately! Cheers and thanks to Daniel and Ken in comments below and to everyone who chimed in on Twitter. 

***

I always account for virally-induced mutation when I imagine the evolution of our genome. That's because I'll never forget this quote. Who could?

“Our genome is littered with the rotting carcasses of these little viruses that have made their home in our genome for millions of years.” - David Haussler in 2008 

Or this...

"Retroviruses are the only group of viruses known to have left a fossil record, in the form of endogenous proviruses, and approximately 8% of the human genome is made up of these elements." (source and see this)

Exciting virus discoveries aside, we're constantly mutating with each new addition to the human lineage. Thanks to whole genome sequencing, the rate of new mutation between human parent and offspring is becoming better known than ever before. We each have new single nucleotide mutations in the stretches of our DNA that are known to be functional (very little of the entire genome) and that are not (the majority of the genome). These are variants not present in our parents’ codes (for example, we might have a ‘T’ where there is a ‘A’ in our mother’s code). And there are also deletions and duplications of strings of letters in the code, sometimes very long ones. Estimates vary on parent-offspring mutation rate and that's because there are different sorts of mutations and individuals vary, even as they age, as to how many mutations they pass along, for example. Still, without any hard numbers (which I've left out purposefully to avoid the mutation rate debate), knowing that there is constant mutation is helpful for imagining how evolution works. And it also helps us understand how mutations even in coding regions aren't necessarily good nor bad. Most mutations in our genome are just riding along in our mutation-tolerant codes—where they will begin and where they will go no one knows!

And it's with that appreciation for constant, unpredictable, but tolerated mutation—of evolution's momentum, of a lineage's perpetual change, selection or not—on top of a general understanding of population genetics that just makes adaptation seem astounding. It makes it difficult to believe that adaptation is as common as the myriad adaptive hypotheses for myriad traits suggest.

That's because this new raw material for adaptation, this perpetual mutation, really is only a tiny fragment of everything that can be passed on. But, what's more, each of those itty bitty changes could be stopped in its tracks before going anywhere.

The good, the bad, and the neutral, they all need luck to pass them onto the next generation. That's right. Even the good mutations have it rough. Even the winners can be losers! Here are the ways a mutation can live or die in you or me:

The Brief or Wondrous Life of Mutations, Wow.

This view of mutation fits into that slow and stately process that Darwin described, despite his imagination chugging away before he had much understanding of genetics.

Of course, bottlenecks or being part small populations would certainly help our rogue underdogs proliferate, and swiftlier so, in future generations.

Still, trying to imagine how any of my mutations, including any that might be adaptive, could become fixed in a population is enough to make me throw Origin of Species across the room.

By "adaptive," I'm talking about "better" or "advantageous" traits and their inherited basis ... that ever-popular take on the classic Darwinian idea of natural selection and competition.

For many with a view of mutation like I spelled out above, it's much easier to conceptualize adaptation as the result of negative selection, stabilizing selection, and tolerant or weak selection than it is to accept stories of full-blown positive selection, which is what "Darwinian" usually describes (whether or not that was Darwin's intention). One little error in one dude's DNA plus deep time goes all the way to fixed in the entire species because those who were lucky enough to inherit the error passed it on more frequently, because they had that error, than anyone passed on the old version of that code? I guess what I'm saying is, it's not entirely satisfying.

But what if a mutation could be less pitiful, less lonely, less vulnerable to immediate extinction? Instead, what if a mutation could arise in many people simultaneously? What if a mutation didn't have to start out as 1/10,000? What if it began as 1,000/10,000?

That would certainly up its chances of increasing in frequency over time, and quickly, relative to the rogue underdog way that I hashed out in the figure above. And that means that if there was a mutation that did increase survival and reproduction relative to the status quo, it would have a better chance to actually take over as an adaptation. This would be aided, especially, if there was non-random mating, like assortative mating, creating a population rife with this beneficial mutation in the geologic blink of an eye.

But how could such a widespread mutation arise? This sounds so heartless to put it like this, but thanks to the Zika virus, it seems to me that viruses could do the trick.

Electron micrograph of Zika virus. (wikipedia)

I'd been trapped in thinking that viruses cause unique mutations in our genomes the way that copy errors do. But why should they? If they infect me and you, they could leave the same signatures in our genomes. And the number of infected/mutated could increase if the virus is transmitted via multiple species (e.g. mosquito and human, like Zika). If scientists figure out that the rampant microcephaly associated with the Zika virus is congenital, wouldn't this be an example* of the kind of large-scale mutation that I'm talking about? 

*albeit a horrifying one, and unlikely to get passed on because of its effects, so it's not adaptive whatsoever.

If viral mutations get into our gametes or into the stem cells of our developing embryos, then we've got germ-line mutation and we could have the same germ-line mutation in the many many genomes of those infected with the virus. As long as we survive the virus, and we reproduce, then we'll have these mutant babies who don't just have their own unique mutations, but they also have these new but shared mutations and the shared new phenotypes associated with them, simultaneously.

Why not? Well, not if there are no viruses that ever work like this.

We need some examples. The mammalian placenta, and its subsequent diversity, is said to have begun virally, but I can't find any writing that assumes anything other than a little snowflake mutation-that-could.

Anything else? Any traits that "make us human"? Any traits that are pegged as convergences but could be due to the mutual hosting of the same virus exacting the same kind of mutation with the same phenotypic result in separate lineages?

I've always had a soft spot for underdogs. And I've always given the one-off mutation concept the benefit of the doubt because I know that my imagination struggles to appreciate deep time. What choice do you have when you think evolutionarily? However, just the possibility that viruses can mutate us at this larger scale, even though I know of no examples, is already bringing me a little bit of hope and peace, and also some much needed patience for adaptationism.

***

Update: I just saw this published today, asking whether microcephaly and other virus-induced birth defects are congenital. Answer = no one knows yet: http://www.nytimes.com/2016/02/09/science/zika-virus-microcephaly-birth-defects-rubella-cytomegalovirus.html?partner=IFTTT&_r=1

Bakarmısın ?

Blog tanıtımları...

 Tık tık Tediş

Merhabalar aslında   şimdiye kadar hiç blog tanıtmadım , tanıtmayı yapamam diye hiç bulaşmadım. Herkesin bir  işi vardır kimi güzel yazamaz , kimiz güzel biçemez kimi  falan kimi  pişman :)) Allah utandırmasın diyorum  . Bu gün bir yorumuma cevaben  bana  yazan arkadaşımın kelimelerinden sonra  bencil olduğumu hissettim ve bu güzel insanı herkesin tanımasını istedim.

 O bir anne hemde çok özel bir anne  , sizi gelip her yazınızı okuyamayabilir , her yazınıza yorum yapamayabilir.

 Dedim ya o çok özel bir anne  yazdıklarından çok bilgiler öğrenebilirsiniz, ben   face'de blogcanlar grubunda görmüştüm yazısını ve resim ilgimi çekmişti Sevgili  Tediş ,  bloğuna girip  bir solukta tüm yazılarını okudum ziyaret etmenizi tavsiye ederim o benim    blog kardeşim ....

 Zaten huyumdur , bir bloğa ilk defa gidiyorsam okuyabildiğim kadarını mutlaka okurum , Mevlüdenin bloğuna ilk girdiğimde bazı paylaşımlarında,   yüz felci geçiriyorum dedim  gülmekten,  Mevlüde demişken araya onuda katmazsam olmaz :)

 Nasıl güzel şeyler biçip dikiyor  mutlaka görmelisiniz , helede anlatımı  müthiş...

 tık tık Mevlüde 

  

Ve Can dostum Melek yaz gelsede  yine sarılsam diyorum:)) özledimmmm:)

 O benim can dostum her gün elli defa  konuşup yazıştığım  dert ortağım, sırdaşım  ablam herbişeyim işte:))

tık tık  Allah-ne-verdiyse 

 Vee o ilk  okuduğumda hayran olduğum annelerden bir diğeri, iki çocukla her şeye zaman bulabilen  genç bir anne , çocuklar konusunda bir çok  bilgiye ulaşabilirsiniz. 

 İlk anne çocuk bloğu olarak eklediğim blogtu  hemen hemen her yazısını okumuşumdur , çocuklar konusunda bir şey kafanıza takılıyorsa mutlaka uğramalısınız... 

Tık tık 2 çocukla hayat

Not:  Umarım yapabildim , Tanıtımını isteyen arkadaşları seve seve tanıtırım umarım yüzüme gözüme bulaştırmam:)

Bizim Hikayemiz # 3 #

Kalp ağrıları...

O bensiz mutluydu böyle istiyordu varlığım onu rahatsız ediyordu. Hayatıma devam etmek zorundayım Derya ile evleniriz diye kenara attığım paraları umarsızca harcıyorum. Bütün kadınlar bayılırken o pembe rengi sevmezdi , gidip kendime pembe kanepe takımı ve onu tamamlayacak sehpalar ve objeler aldım. Evime gelen erkek arkadaşlarımın alaylarına maruz kalsam da çok memnundum, kızlar bayılıyor, sonuçta yeni kızlar yeni ilişkiler kuruyordum , ancak uzun soluklu olmuyor, hiç bir ilişkiyi ciddiye almıyor, çoğu zaman bu ilişkiler günlük oluyordu , tabii buna gönül ilişkisi denirse... 

Uzun soluklu bir Günlük ilişkiler yaşıyordum, insanların aciz olduğunu düşünüyorum, çıkar ilişkisi , bende neyi bulamadım , düşünmeden edemiyorum eksik olan neydi, her istediği oluyordu hatta fazlası ,aklıma tek gelen şey dış görünüşümü beğenmedi daha yakışıklı birini arıyordu.

 Her hafta sonu gizli gizli iş yerinin önüne gidiyor saatlerce karşıdan onu izliyorum , dükkanlarının önü boydan boya camekan olduğu için aklıma onu arayıp telefonda benim numaramı gördüğündeki yüz ifadesini görmek istemiştim .  

Telefonumdan numarasını bulup aramaya bastım telefonu kapalıydı ,karşıdan görüyordum telefonuyla oynuyor bir yerlere bakıyordu. sanırım hattını değiştirmişti, kısacası aramamı istemiyordu. benim ise ondan kolay kolay vazgeçmeye niyetim yoktu.

Aradan sekiz ay geçmişti , pazar günü ben ve yalnızlığım bir hafta sonu pembe kanepe takımının en büyük olanına uzanmış kitap okuyordum cep telefonum çaldı hemen baktım , belki odur diye hala umut var içimde. Nasıl bir duygu bu hiç bir zaman aramayacağını bile bile...

Yabancı bir numaraydı önemsemedim, biraz çalıp durdu. Ve tekrar çalmaya başladı arama düşene kadar ısrarla çaldırışlarına dayanamayıp açtım 

''alo alo deniz hanımla görüşecektim'' 

kızmıştım Deniz hanım kalmadı , bey verelim.

''ah pardon Deniz bey özür dilerim , ben Hüsniye bakın nasıl söyleyeceğim bilmiyorum ama başınız sağ olsun anlamadım neyi oluyorsunuz bilmiyorum ama bir akrabanız sanırım , vefat etti belediye kimsesizler mezarlığına gömecekti ama ben cüzdanında numaranızı buldum , verdiğim adrese lütfen gelir misiniz''

Dolandırıcı olunur da bu kadarına da pes kardeşim 

deyip yüzüne kapadım .

Israrla arıyor açmayınca adresi mesaj olarak atıp ayıp be defin parasından mı kaçıyorsun ben öderim mezarına su dökmeye git bari su dökmekten de başka şey anlarsın şimdi odun...

Odun mu , merakımdan aracıma binip adrese uzaktan bakmaya karar verdim ...

Adrese yaklaştığımda kalabalık fazlalaşmıştı bir şeylerin olduğu belliydi aracımı bir kenara park edip adrese gittim. Telefondaki ses doğru söylemişti bir cenaze vardı fakat ben tanımıyordum bilmediğim bir akrabam mıydı acaba...

müstakil bahçeli bir evdi komşular toplanmış kimi bahçede kimi içeride laflıyorlar , beni yabancı görünce bir kaç kadın. Bana gözlerini dikti hemen konuşmaya başladım , pardon beni bu adresten Hüsniye diye bir hanım aradı, kadınlardan olaya vakıf olduğu belli olan şişmanca başına taktığı beyaz örtüyle , beyaz yüzü ortaya çıkan uzun elbiseli bir kadın ''Hüsniye bak kızım , Didarın oğlu geldi'' dediğinde şok geçiriyordum bir annem mi vardı yıllardır anne sandığım insan annem değildi ,o öldü diye üzülürken ikinci anneyi kaybetme acısını yaşayacaktım . 

Bir anda sudan çıkmış balık gibi oldum kapıdan yirmili yaşlarda ince uzun , esmer tenli bir kadın ''efendim anne ''dedi Annesi olduğunu anladığım kadın yüzüme tiksinir gibi bakarak ''bak aradığın adam geldi'' , kızgın kızgın yüzüme baktı ve arkasını dönüp dışarı çıktı.

Hüsniye Hanım içeri girerken bende onu takip ediyordum, tur rehberi edasındaydı , onu takip ediyor şaşkınlığımdan ne diyeceğimi bilemiyordum bir şeyler dediğimde duruyor yüzüme dönüp cevap veriyor sonra yine umursamaz hareketlerle işine devam ediyordu arada o durup bana dönüyor ben yürümeye devam ettiğimden çarpışır gibi oluyor istersen öp diye tersliyordu ne tuhaf biri . olayın böyle saçma hal almasından sıkılıp arkası dönükken kolundan tuttum ve Hüsniye hanım bakın ben bir annem olduğunu bile bilmiyordum .

'' o da çok gururluydu hiç bir zaman sizden bahsetmedi'' diyor ancak gözlerime hiç bakmıyordu , bahsetmediyse peki siz nasıl biliyorsunuz o zaman , taziyeye gelenlere ikramda bulunuyor ,bende peşinde bir bahçeye bir içeri geziyor , hemde anlamaya çalışıyordum tepsi elinde durdu ve birden sırtına yapıştım utandım, bana dönüp '' bana bak didar teyze on beş yıldır burada oturuyor ev sahibi kirayı bile arttırmaz çok iyi biriydi ve çok fakir üç aylık maaşıyla geçinirdi,gururundan söylememiş aramamış sizi besbelli bir derdi vardı ama hiç birimiz bilemedik.''

Tamam ama ben bilmiyordum peşinde gezerken birden salonda çerçeveli bir resim gözüme çarptı hey dur dur biraz , bu kadın annem olamaz ki ''ne oldu aşağılıyormusun! çok kabasın'' , iyide bu kadını ben bir gün moralim bozuktu benimle konuştu ve çocuğum olmayacak diye illa numaramı istedi bende verdim hepsi bu ''hmm çocuğunuz olmuyor demek '' yok yanlış anladınız sizde , evli değilim ben .Başka bir şey kastetmiştim... Yani kız arkadaşım benimle evlenmediği için yani , şey hani evlenmezse nasıl olur , işte saçmalamaya başlamış yüzüm kıpkırmızı olmuştu.

Gülümsedi birden ''tövbe yarabbi cenaze evinde güldürdünüz beni , hiç bir alakanız yok, zaten biz komşular kendi aramızda para topladık duası için sizden umudu kesmiştik .''

Öderim dedim karşılıklı itirazlardan sonra ödemek istediğimi içimden gelerek yaptığımı kabul ettirdim duası ve ikramları derken saat geç olmuştu komşular bir bir ayrılırken Hüsniye ve annesi kaldı sadece.

Hüsniye madem bir bağınız yok eşyalarını ikinci el satın alan yerlere , anahtarı da ev sahibine biz teslim ederiz ... 

bütün gün peşinde gezdiğim kadını merak etmiştim . Eşiniz gelmedi dedim sırf vereceği cevabı merakımdan acaba Didar hanım teyzenin şu doktoru bulan komşusumuydu yoksa , sesini çıkarmadı o ara annesine emirler yağdırıyordu durmadan '' camlarını kapadın mı , ocağı kontrol ettin mi?'' Yaşlı kadında uslu küçük bir çocuk gibi uyguluyordu .İşleri bitince , bahçe kapısına kadar birlikte çıktık , ben karşıya geçip aracıma binip tam çalıştırdığımda karşıdan bana el hareketiyle aracın camını aç diye işaret yaptı, camı açtım benimde hiç çocuğum olmayacak deyip koşarak , kendi evlerine ilerlemekte olan annesinin koluna girip karanlığa karıştılar , arkasından öylece baka kaldım eve gelip duş, traş ikilisinden sonra kendimi yatağa attım ne gündü ve Hüsniye beni anlamıştı ne demek istediğimi anlamıştı demekki o da yaralıydı... Sabah uyandım aklımda Hüsniye , neyi mazeret edip görüşebiliriz diye bütün gün teoriler ürettim.

çekiliiş var:)))

 Merhabalar

 öncelikle  iyiyim diyelim iyi olalım:)

 Gecikmelide olsa çekilişime başlıyorum  sevgili visnelikiraz'ımın  başlattığı bir çekilişti. bende çok güzel hediyeler kazanmıştım.

 ve  aynı çekilişi bende devam ettiriyorum, hem çekiliş hem kampanya gibi bir şey aslında:)
 amaç ,   bir çok blogta  aşağıdaki resim görülsün ,sesimiz duyulsun,
sadece  sokak hayvanları için bir şeyler yapmaya çalışıyorum 

   Sokak hayvanlarına  bir kap yemek bir kap su kampanyası ,Yani çekilişe katılmak istemeyeni kampanyamıza katılmasını rica ediyorum. Sesimizi duyurmak için siz sevgili dostlara ihtiyacımız var.

 Uzatmadan çekiliş hediyeleri huzurlarınızda:) 

 Kitapları sahaftan aldım  ve dove'nin seyehat seti, özel imalat bir yüzük....

  

Katılım için  bloğa üye olup olmamanız çokta önemli değil,    çekilişi kendi bloğunuzda  paylaşmanız, duyurmanız yeter,

Blogunuzda görseli ile çekilişi paylaşmak  bloğu olmayan arkadaşlar hayvan dostlarımıza yaptığı desteği kareleyip aşağıdaki adresime mail atmaları yeterli . Örneğin kuşlara koyduğu yemi sokağa bıraktığı suyu bunun gibi şeyler.

 ,yoruma mail adresinizi bırakabilirsiniz, yoruma katıldığını  bana bildirenler arasından çekilişle  kazananlar belirlenecek, kargo bana ait  

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Paylaştığınız linkleri yoruma yazmayanlar dikkate alınmayacaktır.

The Primate Family Tree: A classroom activity in evolution, adaptable for all ages

Feel free to email me to request the document (with all this text and all these figures) which is easier to work with. holly_dunsworth@uri.edu

In this activity, students will…

• Observe and describe the similarities and differences between primates and other familiar mammals, and also the similarities and differences among primates.

• Classify primate species into groups (superfamily and above). 

• Transform Linnaean classification into evolutionary theory by merely changing the question from How do primates look similar and different from one another? to Why do primates look similar and different from one another?

• Build a primate “family” tree by turning Linnaean classification into phylogeny (or evolutionary tree-thinking) to describe how common ancestry and change over time explain both similarities and differences among primates.

How old are the students? 

5-105* 

*Prior to about age 8, teachers will need to riff quite creatively off track from this (for one, because reading the Primate Taxonomy Table may be very difficult for younger students), but I include those earlier ages because I believe that teachers of those age groups can find a way to use this lesson if they’d like to. It's possible that just knowing how to read is enough to do a stripped down version of this activity, which includes children even younger than 5. I have used this activity successfully with students aged 8-25. For upper-level anthropology courses I've used it as an ice-breaker to kick off the semester (with students who have a background in evolutionary thinking already).

How long will it take? 

30 minutes minimum (much more depending on detail you wish to cover)

What materials?

• Color pictures of a diverse array of primates - approximately 3-5 times as many pictures as students. Too many is better than too few. Rip them out of old textbooks and laminate for durability. Print them off the Internet (arkive.org is one of the best sources) and laminate for durability. Make sure to have at least two different pictures of the same species for many of the species you include. Label most of them with the common names under “examples” on the chart for Part 2 (e.g. “baboon”). But a fraction may be only labeled with geographic region, scientific name, or nothing at all.  Explanation is in the instructions below. Specific sources of primate photos for printing are listed in Appendix A.

• Pencil – 1 per student

• Note cards -  1 per student (for them to draw a self-portrait or a symbol to represent themselves)

• Poster paper, or large sheets of paper – 6, one for each superfamily on the Primate Taxonomy Table (below)

• Tacky gum, reusable tape, or some other ingenious sticky tool that can both hold primate pictures to the posters and also be removed and moved to different posters when students change their minds. 

• Handout for students (see options below; must at minimum include Part 2: Primate Taxonomy Table)

 

Teacher Instructions

Part 1. (3 MINUTES minimum) DISCUSS CLASSIFICATION

Using the resources under Part 1 of the materials below, hold a discussion about classification. Don’t talk about relatedness or common ancestry! And especially don’t talk about evolution! (Next, in Part 2, the taxonomic terminology they will use, like “family,” will encourage them to think evolutionarily, hopefully, and this will come into play later in the activity.)  They will already be familiar with how like is grouped with like—I often use sock and underwear drawer analogy, grocery store organization works too. Stick to primates if you’d like, but if you go broader, make sure to end your discussion with primates, including humans. Make sure to explain how (Linnaean) taxonomy/classification works. That is, simply/broadly (or complicated/specifically if you’d like) describe the methods—the use of comparative anatomy and homology and also the binomial species name for the smallest, most exclusive group within ever-more inclusive groups going up to the Kingdom level.

Part 2. (10 MINUTES minimum) CLASSIFY THE PRIMATES INTO SUPERFAMILIES

Hang a poster for each superfamily along the wall in no particular order, lay out a pile of the photos in no particular order. Students get up out of their chairs, and using the Primate Taxonomy Table (below) they stick each primate picture to a poster labeled with the superfamily to which they think it belongs. They are able to do this without any knowledge of primates because you have labeled most of the pictures with “baboon”, for example. They can go to the table on the handout and see that baboons belong in the superfamily “cercopithecoidea” and stick the photo to that poster. Unlabeled baboons should look similar to labeled ones and they should also be sticking those to the cercopithecoidea poster if they are carefully observing and are engaged in the activity. Make sure they stick their own “human” cards to a poster too.  Hopefully they will respectfully work together and move others’ around if they think they have a better case for a different classification of a particular primate.  

Primate Taxonomy Table (handout).
Email me for a file you can work with more easily (holly_dunsworth@uri.edu)

Part 3. (5 MINUTES minimum) STUDENTS SHARE THEIR REASONING FOR THEIR CLASSIFICATION

Lead the students through a tour of the features that unite the primates into each of the superfamilies. First ask them to describe the similarities among all the primate superfamilies (a quick review of Part 1). Then ask them to describe the differences they can see between the superfamilies: what makes hominoids separate from cercopithecoids, etc?  It’s not imperative, but I recommend starting with the primates that share the most with humans (hominoidea) then going to the cercopithecoidea, and so on. This may appear to be difficult because they may observe overall (super) family resemblance but not be able to describe any more detail than that, which is fine! Using the resources under Part 3 below, you can provide details of the differences between the superfamilies, both that are visible in the pictures and that are not. 

Part 4. (2 MINUTES minimum) CHANGE THE QUESTION FROM HOW DO PRIMATES VARY? TO WHY DO PRIMATES VARY? 

Challenge students to explain the patterns of similarities that make all these creatures primates and that, for example, unite the hominoids, the cercopithecoids, etc..., while also explaining the differences that make each species unique and each superfamily unique.  Hopefully, with very little help from you, they will arrive at the idea that relatedness explains it. Family history, on a larger scale than our own families, but the same kind of thing. Common ancestry and change over time since common ancestors. Evolution plain and simple.  

Part 5. (10 MINUTES minimum) BUILD A PRIMATE TREE and DISCUSS ITS MEANING. 

There are many ways to do this and showing more than one way would be great, but one way is to put the known phylogenetic structure, the branches of the tree for the superfamilies (see resources below) on the wall or board and have them deduce where the superfamilies go and stick the posters to those branches. Another way, for older students, is to have them figure out the relatedness of superfamilies first, starting with humans and hominoids and hypothesizing which are more and more distantly related based on increasing differences. Another is to merely show them how to walk through the table for Part 2, and change it into a hypothesis for phylogenetic/evolutionary history, with lineages diverging where each level of taxonomy divides things further into more exclusive groups. So show them how to draw time and descent lines around that evolution-free taxonomy (classification table for Part 2) that they already have and they’ll arrive at.. dun-dun-DUN evolution! I prefer to draw the students’ hypothesized tree like a big oak tree (with a streps/haplorhine split in the trunk deep down near the bottom) on the wall, and to stick the posters at the ends of the branches. But it’s obviously up to teachers and whether they have a big wall to draw on! I cover my wall in paper first so that I can draw the big tree. 

Teacher Resources and Optional Handout Materials

Teachers: Pick and choose what you’d like to include in your handout, depending on what you will cover with your particular students (depending on age, time, goals, etc…). Be careful not to share any handouts too soon and spoil the opportunity for students to think first, if that’s what you have time for and are going for. 

Part 1

• Where do humans fit in the classification of life on Earth? (link)
• How do we make these categories? We ask, ‘What’s similar” of the anatomy, when comparing different species.  That is we look to homologous structures.  A great example is the tetrapod forelimb. (link)

• What makes a primate a primate? (link)

Part 2

Lemuroidea

Nose: wet (hence the name strepsirrhine)

Geographic region: Madagascar

Tail present: yes

Activity: Some nocturnal, some diurnal

Teeth: Many more than we have, some shaped like comb for grooming fur

Body size: Small but variable from the smallest primate alive (<< 1 lb.) to ones as big as big pet cats (20 lbs.)

Lorisoidea

Nose: wet (hence the name strepsirrhine)

Geographic region: Sub-Saharan Africa and Southeast Asia

Tail present: yes and no

Activity: nocturnal

Teeth: Many more than we have

Body size: small

Tarsioidea

Nose: dry (hence the name haplorhine) 

Geographic region: Southeast Asia

Tail present: yes

Activity: nocturnal

Teeth: Many more than we have

Body size: small

Ceboidea

Nose: dry (hence the name haplorhine) 

Nostrils: flat and facing out to the side (hence the name platyrrhine)

Geographic region: Central and South America

Tail present: yes (and some are even prehensile!)

Activity: Most diurnal, some nocturnal

Teeth: four more than humans (one extra premolar/bicuspid in each quadrant of mouth compared to us)

Body size: Variable, with some small (like pygmy marmosets) but the largest, the spider monkey, is 25 lbs.

Cercopithecoidea

Nose: dry (hence the name haplorhine) 

Nostrils: facing down (hence the name catarrhine)

Geographic region: Asia, Southeast Asia, and Africa (all sub-Saharan except the Barbary macaque of Morocco and Gibraltar)

Tail present: yes (but 2-3 species are no or have very small stubs)

Activity: diurnal

Teeth: same number as humans

Body size: Many, including most macaques and baboons, weigh more than any ceboids. Some mandrills weigh over 100 lbs.!

Hominoidea

Nose: dry (hence the name haplorhine) 

Nostrils: facing down (hence the name catarrhine)

Geographic region: Southeast Asia (gibbons, siamangs, orangutans); Sub-Saharan Africa (gorillas, chimpanzees, bonobos); Worldwide (humans)

Tail present:  no

Activity: diurnal

Teeth: same number as humans

Body size: Although gibbons and siamangs are the smallest of the group, this group is the largest in body size and weight of all primate superfamilies and includes gorillas, the largest of all primates which can weigh 400 lbs.!

Part 4

Evolution and phylogenetic thinking is just family history writ large.

Part 5. The Primate Family Tree

Here is an example (one hypothesis, if you will) of a primate phylogeny or phylogenetic tree or evolutionary tree. 

Here's guidance on how to turn Part 2’s table into a phylogeny with students.

Then here it is, stripped down and rotated...

Appendix A.

Sources for primate pictures

Lemuroidea

Dwarf lemurs: http://www.arkive.org/explore/images?q=Dwarf%20lemurs

Mouse lemurs: http://www.arkive.org/explore/images?q=Mouse%20lemurs

Aye-ayes: http://www.arkive.org/explore/images?q=Aye-ayes

Indris: http://www.arkive.org/explore/images?q=Indris

Sifakas: http://www.arkive.org/explore/images?q=Sifakas

Lemurs: http://www.arkive.org/explore/images?q=Lemurs

Sportive lemurs: http://www.arkive.org/explore/images?q=Sportive%20lemurs

Lorisoidea

Galagos: http://www.arkive.org/explore/images?q=Galagos

Lorises: http://www.arkive.org/explore/images?q=Lorises

Pottos: http://www.arkive.org/explore/images?q=Pottos

Tarsioidea

Tarsiers: http://www.arkive.org/explore/species?q=tarsier

Ceboidea

Howler monkeys: http://www.arkive.org/explore/images?q=Howler%20monkeys

Spider monkeys: http://www.arkive.org/explore/images?q=spider%20monkey

Owl monkeys (night monkeys): http://www.arkive.org/explore/images?q=Owl%20monkeys%20night

Marmosets: http://www.arkive.org/explore/images?q=Marmosets

Tamarins: http://www.arkive.org/explore/images?q=Tamarins

Capuchins: http://www.arkive.org/explore/images?q=Capuchins

Squirrel monkeys: http://www.arkive.org/explore/images?q=Squirrel%20monkeys

Titi monkeys: http://www.arkive.org/explore/images?q=Titi%20monkeys

Sakis: http://www.arkive.org/explore/images?q=Sakis

Uakaris: http://www.arkive.org/explore/images?q=Uakaris

Cercopithecoidea

Baboons: http://www.arkive.org/explore/images?q=Baboons

Macaques: http://www.arkive.org/explore/images?q=Macaques

Vervets: http://www.arkive.org/explore/images?q=Vervets

Guenons: http://www.arkive.org/explore/images?q=Guenon

Colobus: http://www.arkive.org/explore/images?q=Colobus

Langurs: http://www.arkive.org/explore/images?q=Langurs

Proboscis: http://www.arkive.org/explore/images?q=proboscis%20monkey

Drills and mandrills: http://www.arkive.org/explore/images?q=drill%20mandrill

Hominoidea

Gibbons: http://www.arkive.org/explore/images?q=Gibbons

Siamangs: http://www.arkive.org/explore/images?q=Siamangs

Orangutans: http://www.arkive.org/explore/images?q=Orangutans

Humans: students draw a personal sign, symbol, or self-portrait

Chimpanzees: http://www.arkive.org/explore/images?q=Chimpanzees

Bonobos: http://www.arkive.org/explore/images?q=bonobo

Gorillas: http://www.arkive.org/explore/images?q=Gorillas

Paradise

 Porthgwarra to Rospletha Cliffs......

  dramatic, wild and beautiful.

 Forget your tropical islands.....for me this is paradise

Where in the world is your little corner of paradise?

Thoughts on the latest schizophrenia genetics report

The news and social media were headlining a report last week that presented some genetic findings, and even aspects of a possible causal mechanism, related to schizophrenia.  As habitually skeptical readers of these daily stories, we wondered how substantial this claim is.

The report in question was a Nature paper by Sekar et al. that identifies variation in the very complex MHC genome region that, based on the authors' analysis, is statistically associated with schizophrenics relative to unaffected controls. These are variants in the number of copies of particular genes in the C4 'Complement' system.  The authors show that gene copy number is correlated with gene expression level and, in turn, with some changes in brain tissue that may be related to functional effects in schizophrenia patients.

Comparing genotypes and disease status, in ~30,000 cases and controls of European ancestry, in 40 cohorts from 22 countries, the authors find that genotypes with higher C4 gene copy numbers are more frequent in schizophrenics, and there is a quantitative relationship between copy number and expression level in postmortem-tested neural tissue.  The relevant potential mechanism involved may have to do with the pruning of synapses among neurons in the brain.

The authors estimate that the relative risk of the highest-copy number genotype is 1.27 times that of the lowest. The lowest risk genotype is rare in the population, comprising only about 7% of the sample population, meaning that almost everyone has a middling relative-risk genotype.  That is comparable, say, to most of us having middling height or blood pressure. But the net population absolute risk of schizophrenia is about 1%, so that the absolute risks associated with these various genotypes are small and not even very different from each other.  The careful work done by the authors has many different components that together consistently seem to show that these copy number differences do have real effects, even if the absolute risks are small.

How that effect or association arises is not clear, and the findings are certainly not the same as explaining schizophrenia as a C4 disease per se.  As the authors note, around 100 or so other chromosome locations have been associated with the disease in genome-wide mapping studies that have been done.  That means that if their results stand up to scrutiny, C4 variation is one component of what is basically a polygenic disorder.  The association for each C4 genotype category is the effect averaged over all other contributing causes in those people. The absolute risk in individuals with a given copy number is still very small, and may depend on other genetic or environmental factors.

Schizophrenia is not a single disorder and has a spectrum of onset age, sex, symptoms, and severity of occurrence.  Many authors have been warning against using a single term for this variety of traits. Whether that is relevant here or not remains to be seen, but at least as presented in the their paper, some of the current authors' results seem not to vary with age.  This study doesn't address whether there is a smallish subset of individuals in each C4 category who are at much higher risk than the average for the category.  However, the familial clustering of schizophrenia suggests this may be so, because family members share environments and also genomic backgrounds.  One might expect that C4 genotypes are interacting with, or if not, being supplemented by, many other risk factors.

Even if average risk is not very high in absolute terms, this paper received the attention it did because it may be the first providing a seemingly strong case for a potentially relevant cellular mechanism to study, even if the specific effect on risk turns out to be quite small.  It could provide a break in understanding the basic biology of schizophrenia, given the dearth of plausible mechanisms know so far.

Because the statistically riskier genotypes are found in a high percentage of Europeans, one would expect them to be found, if at varying frequencies, in other populations than Europeans. Whether their associated risks will be similar probably depends on how similarly the other risk factors are in other populations.  C4 copy number variation must be evolutionarily old because there is so much of it, clearly not purged by natural selection--another indicator of a weak effect, especially because onset is often in the reproductive years and would seem to be potentially 'visible' to natural selection. So why is the C4 variation so frequent?  Perhaps C4 provides some important neural function, and most variation causes little net harm, since schizophrenia is relatively rare at roughly 1% average risk.  Or, copy number changes must happen regularly in this general MHC genome region, and can't effectively be purged, but is generally harmless.  But there is another interesting aspect to this story.

The Complement system is within a large, cluster of genes generally involved in helping destroy invading pathogens that have been recognized.  It is part of what is called the 'innate' immune system. Innate here means it does not vary adaptively in response to foreign bodies, like bacterial or viruses, that get into the blood stream.  The adaptive immune system does that, and is highly variable for that reason; but once a foreigner is identified, the complement system takes part in destroying it.  So it is curious that it would be involved in neural degeneration, unless it is responding to some foreign substance in the brain, or is an autoimmune reaction. But if the latter, how did it become so common?  Or is the use of C4 genes in this neural context a pleiotropy--a 'borrowed' use of existing genes that arose for immunity-related functions but then came also to be used for a different function?  Or is neural synapse regulation a kind of 'immune' function that hasn't been thought of in that way?  Whatever it's doing, in modern society it contributes to problems about 1% of the time, for reasons for which this paper clearly will stimulate investigation.

Why does this system 'misfire' only about 1% of the time?  One possible answer is that the C4 activity prunes synapse connections away normally in a random kind of way, but occasionally, by chance, prunes too much, leading to schizophrenia.  The disease would in that sense be purely due to random bad luck, rather than interacting with other mechanisms or factors. The higher the copy number the more likely the bad luck but too weakly for selection to 'care'.  However, that reason for the disease seems unlikely, for several reasons.  First, mapping has identified about 100 or so genome regions statistically associate with schizophrenia risk, suggesting that the disease is not just bad luck. Secondly, schizophrenia is familial: close relatives seem to be at elevated risk, 10-fold in very close relatives and almost 50-fold in identical twins.  This should not happen if the pathogenetic process is purely random, even though since haplotypes are inherited in close family members there could be a slight correlation in risk.  Also, the authors cite several incidental facts that suggest that C4 plays some sort of systematic relevant functional role.  But thirdly, since the absolute risk is so small, about 1%, one has to assume that C4 is not acting alone, but is directly interacting with, or is complemented by (so to speak) many other factors to which the unlucky victims have been exposed.

Something to test?
This might be a good situation in which to test a variant of an approach that British epidemiologist George Davey Smith has suggested as 'Mendelian randomization'.  His idea is basically that, when there is a known candidate environmental risk factor and a known gene through which that environmental factor operates, one can compare people with a genetic variant exposed to an environmental risk factor to people with that genetic risk factor but not exposed to test whether the environmental factor really does affect risk.

Here, we could have a variant of that situation.  We have the candidate gene system first, and could sort individuals having, say, the highest 'risk' genotypes, compared to the lowest, and see if any environmental or other systematic genomic differences are found that differentiates the two groups.

Interesting lead but not 'the' cause
Investigating even weakly causal factors could lead the way to discovering major pathogenic mechanisms or genetic or environmental contributors not yet known that interact with the identified gene region. There will be a flood of follow-up studies, one can be sure, but hopefully they will largely be focused investigations rather than repeat performances of association studies.

Given the absolute risks, which are small for given individuals, there may or may not be any reason to think that intervening on the C4 system itself would be a viable strategy even if it could be done. This still seems to be a polygenic--many-factorial--set of diseases, for which some other preventive strategy would be needed.  Time will tell.

In any case, circumspection is in order.  Remember traits like Alzheimer's disease, for which apoE, presenilins, beta-amyloid, and tau-protein associations were found years--or is it decades?--ago and still mystify to a great extent.  Or the critical region of chromosome 21 in in Down syndrome that has, as far as we know, eluded intensive study for similarly long times. And there are many other similar stories related to what are essentially polygenic disorders with major environmental components.  This one is, at least, an interesting one.

Porthgwarra

 J and I have escaped for a little winter break to celebrate our birthday, and we've come to the tiny cove of Porthgwarra on the most south-westerly tip of Cornwall, not far from Land's End. Our holiday cottage is the small low building on the far right. I've never actually had a 'holiday' in Cornwall before! It feels rather nice to experience for oneself what all those holiday-makers come to Cornwall to experience, with the added bonus of being almost alone to enjoy it.

It was too dark to see anything when we arrived last night, so imagine our delight to wake up this morning and see this wonderful view from the sitting room. The seats at the bottom of the garden are perfect for wave-watching, and two seals were having a lovely time in the surf.

 I have never been to this particular part of the coast before......

the granite cliffs are quite spectacular.

 

There are two tunnels through the rock leading to the beach; I'm not sure if they are wholly natural or partly man-made, perhaps as an easier way of  bringing cargo up off the beach as the slipway itself is incredibly steep.

I spent most of today just wave-watching. Perfect.

Hope you too are doing something nice to banish away those winter blues. xxx

We're all fundamentalists now

If you're a foodie at all, you've heard of Yotam Ottolenghi, chef, restauranteur, and food writer.  Perhaps you've used some of his recipes, or even have one or more of his cookbooks. And, if you're a fan you'll be happy to know that the Jan 11 episode of the Food Programme on BBC Radio 4 has an interview with him (starting at minute 7:15), and a brief overview of how he got to such a place of prominence in the food world.  

Ottolenghi and his business partner, Sami Tamimi both come from Jerusalem, but Ottolenghi from the Jewish west side and Tamimi from the Arab west.  They both now live in London where they have collaborated since the late 1990's on restaurants and delis and cookbooks, much of it with the aim of highlighting the food of their childhood.  Not only is their food amazing, but it's also worth noting that two men from two sides of the same strife-ridden Middle Eastern city have worked closely together for many years. This isn't something that everyone could do.   

One of the cookbooks Ottolenghi and Tamimi wrote together is called Jerusalem, written to accompany a BBC television program of the same name. For the show, they returned to their birthplace and described and prepared some of their favorite foods, but it wasn't just about the food.  Tamimi said it was difficult to return. He believes that people were much more naive when he was a child, having faith that the conflict between Israel and Palestine could be solved. Now, he says, people are much more entrenched in their belief in the rightness of their side, and it's much more difficult to imagine the differing sides agreeing on a solution.

To us in the West, the Middle East epitomizes fundamentalism, strict adherence to the literal interpretation of a religious text or dogma.  And, fundamentalism goes hand in hand with terrorism. Fundamentalism is our enemy.

But, it's not just in the Middle East that people are more entrenched in their beliefs about right and wrong. Here in the US we've got the Tea Party dictating what real conservatism is, we've got militiamen in Oregon, and homegrown 'terrorists' demanding whatever they're demanding. We've got a Congress that agrees only to disagree. Dare I say it, even the 'new atheists' are fundamentalists. Indeed, compromise has become a dirty word, immoral even. In so many ways, moderation, the ability to see more than one side of an issue, has lost its way.

Ken's view is that in a world in which fundamentalists are now our enemy, we've all become fundamentalists; we know what we believe, we hold to those beliefs without question, and we have no respect for the other side.  If there is a strongly ideological force that you disagree with or that threatens you, it pushes you toward an equal and opposite ideology. You listen only to Fox News or MSNBC, you turn off the radio when Trump comes on, or when Clinton comes on, depending on your predilection -- or you're waiting for the Libertarian candidate to be selected, and there's no way you'll listen to anyone else.

If you're here reading this it's likely that you've also picked a side in the nature/nurture 'debate'; 'genetic determinism' either nicely describes your view of biology, or you're very uncomfortable with the term. Genes will or will not be found 'for' most traits, including behaviors, and diseases will or won't be predictable once we've all got our genomes on a CD.

We've said this before but it's worth repeating.  In 1926, one of the great early geneticists, Thomas Hunt Morgan, wrote this about stature:

A man may be tall because he has long legs, or because he has a long body, or both. Some of the genes may affect all parts, but other genes may affect one region more than another. The result is that the genetic situation is complex and, as yet, not unraveled. Added to this is the probability that the environment may also to some extent affect the end-product.
                                  (TH Morgan, The Theory of the Gene, p 294, 1926):

Morgan would be totally comfortable with the recent GWAS results showing that there are hundreds if not thousands of genes that contribute to stature, as well as environmental factors.  He'd agree that complex traits, like stature, or many diseases (including schizophrenia, which Ken will talk about tomorrow) are polygenic, with some environmental effect.  This has been known for almost a century. So why are people still looking for genes (meaning single genes, or a few genes with individually strong effects) 'for' type 2 diabetes, or heart disease, or stature, or schizophrenia?  Why don't we still know what Morgan knew so long ago?

Because sometimes it's not true.  Sometimes there are single genes whose variants are by themselves responsible for traits, including disease.  Starting in the early 1980's, the role of single genes in various traits began to be discovered; oncogenes, Huntington's, cystic fibrosis, breast cancer, and a whole host of single-gene pediatric diseases, and normal traits as well, like blood types, eye color and so on.  There are now about 6000 rare diseases for which genetic causation appears to be known, or at least claimed.   This history of successes mislead, we would say, geneticists, and others, into assuming they could always expect to find 'the' gene for this and 'the' gene for that.  In essence it is still the informal working model, in the back of geneticists' heads, that everything segregates like Mendel's pea traits.

We can and do have both -- single-gene traits and complex traits due to many genes, or many genes and environmental factors too.  Indeed, there are also traits that are completely environmental -- look at the havoc Zika virus seems to be wreaking, with apparently no help from genes, even if close examination might find some people to be slightly more immune than others. Most viruses are like that.

So, it's curious that even the field of genetics has its fundamentalists.  Every time Ken and I write about complexity, or insufficient understanding of disease causation, or question how we know what we think we know, someone will send us a link to a paper that shows we're wrong because autism, or schizophrenia, or intelligence, or whatever their favorite trait, has been shown to be clearly genetic. Genes, with names, have been found to explain it. Sometimes the comments are so emotionally unrestrained that you'll never see them because we don't publish them.

And, we'll often or even typically look at the paper and realize that we've been reprimanded by a fundamentalist yet again. Autism, schizophrenia, heart disease, stature, intelligence, and so on are just not yet predictable from genes, and, we believe, are unlikely ever to be for reasons we write about all the time.  Ken will discuss the new Nature paper on schizophrenia tomorrow, a paper that got huge amounts of press for finally beginning to explain the disease.  Yes, a paper someone offered to send us when they disapproved of a post Ken had written about the difficulties of predicting disease, proving he was wrong. Which, good as that paper may be, is not the case.

I think if Morgan were to come back to the modern field of genetics, he'd feel as Sami Tamimi did returning to Jerusalem.  I think he'd be nostalgic for his era, when fundamentalists didn't rule the field, geneticists weren't prisoners of Mendel, ideologues who know what they'd find before they even looked. Where, even if things seem rosier in retrospect, and certainly people had preferred views and were not always nice to each other, there was more agreement that things were not yet clearly understood, and complexity was not a dirty word.  I think Morgan would appreciate that some traits are explained more simply than others, but that even those aren't 'simple' -- there are more than 2000 alleles in the CFTR gene that seem to be associated with cystic fibrosis, and this kind of complexity is true of most 'simple' traits.

So, why did the field lose this understanding, and take a turn to fundamentalism?  The answer isn't just that we're in a fundamentalist age, of course.  That it's a lot easier to sell the search for a causal gene than a search for.....we're not really sure what, is a large part of the problem.  But, as a friend says, we should be looking for the molasses that explains biological complexity, that connects causal pathways and processes, which ain't just gonna be a gene, or an environmental risk factor.  It's going to be something we don't yet understand, and continuing to look for 'the' gene for your favorite complex trait is only going to slow down the search.  Acknowledging that what we've learned, and confirmed over and over again since Mendel was rediscovered in 1900, is that most traits are complex -- and unpredictable -- is a crucial step.